Why Gluten Cereal Grains
May Be Hazardous to Your
Discover the benefits of a gluten-free diet in relieving an
the ailments associated with celiac disease, gluten sensit
more than 200 chronic illnesses and conditions, includin
Cancer
Autoimmune disease
Osteoporosis
Brain disorders
Intestinal disease
Chronic pain
Dangerous Grains
Dangerous Grains
WHY GLUTEN CEREAL GRAINS MAY BE
HAZARDOUS TO YOUR HEALTH
James Braly, M.D.
and Ron Hoggan, M.A,
AVERY
a member of Penguin Putnom Inc.
New York
Every effort has been made to ensure that the information contained in this book is complete and accurate. However, neither the publisher nor the authors are engaged in rendering professional advice or services to the individual reader. The ideas, procedures, and
suggestions contained in this book are not intended as a substitute for consulting with
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in this book represent the personal views of the authors and not of the publisher.
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avery
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Copyright © 2002 James Braly, M.D. and Ron Hoggan, M.A.
All rights reserved. This book, or parts thereof may not
be reproduced in any form without permission.
Published simultaneously in Canada
Illustration of Celiac Sprue: Gluten, MHC, and
Intestinal Immunopathology on p. 65 byMichael N. Marsh, copyright © 1992,
is reprinted with his permission.
Library of Congress Cataloging-in-Publication Data
Braly, James,
Dangerous grains : why gluten cereal grains may be hazardous to your health /
James Braly and Ron Hoggan.
p. cm.
Includes index.
ISBN 1-58333-129-8 (aIk. paper)
1. Celiac disease—Popular works. 2. Gluten—Health aspects—Popular works.
I. Hoggan, Ron. II. Title.
RC862.C44B73
2002
2002022748
616.3'99—dc21
Printed in the United States of America
20 19 18 17
Book design by Amanda Dewey
The ideas that shaped this book have come from myriad sources. Thanking the few identified here ensures overlooking the many others who
have contributed their insights and perspectives, and we apologize in advance for these oversights caused by space limitations. Among the many
people who contributed, Don Wiss, Jonathan Wright, Bob Machon, Ashton Embry, Anthony Marini, Garth Benson, and Michael N. Marsh stand
out. Thanks also go to our families; to Betty Hoggan, who contributed her
enduring support and the faith needed to persevere, and to Zack and
Rachel Braly, for their loving support and inspiration.
Thanks should also be directed to the thousands of dedicated gluten
and celiac researchers around the world who have educated and validated
us in our journey of discoveries. In addition, very special thanks must
posthumously go to Dr, Theron Randolph, renowned and beloved food
allergy-clinical ecology pioneer and clinician, who intellectually grabbed
hold over twenty years ago and has yet to let go.
Finally, we are grateful to the many individuals who generously allowed us to include their case histories as representative of our growing
understanding.
CONTENTS
Foreword by Jonathan V. Wright M.D.
Preface
Introduction
ix
xvii
I
1. Grains and People: An Evolutionary Mismatch
18
2. Types of Celiac Disease and Non-Celiac Gluten Sensitivity
36
3. Proactively Determining Your Risk
47
4. Testing for Gluten Sensitivity in All Its Forms
61
5. Life After Gluten
77
6. The Cancer Connection
105
7. Gluten, Molecular Mimicry, and Autoimmune Disease
117
8. Osteoporosis and Gluten
134
9. Brain Disorders and Gluten
/ 44
10. Bowel Diseases and Gluten
160
11. Where to from Here? Research, Theories, and Treatments
169
APPENDIX A.
Common Signs and Symptoms of Celiac Disease
f 81
APPENDIX B.
Hidden Sources of Gluten
! 83
APPENDIX
c. Autoimmune Diseases Frequently Found
in Celiac Disease
186
APPENDIX D.
Comprehensive List of Gluten-Associated
Medical Conditions
APPENDIX E.
Heroic Thinkers and Dietary Biases
187
203
Sources
209
Index
239
FOREWORD
Are Wheat and Other Grains
Making You III?
Religious tradition calls it the "Staff of Life." Most of us eat it every
day. ft's even a phrase from a well-known prayer: "Give us this day our
daily bread," But a growing and undeniable body of research (reviewed
in this book by my friend and colleague James Braly, M.D., and Ron Hoggan, M.A.) tells us that our daily bread [more specifically, wheat and
related cereal grains) may be negatively affecting as many as 90 million
Americans and may be a basic cause of illness for up to 10 million.
How can this be? Haven't we been told, over and over and over again,
that grains, particularly whole grains, are a fundamental part of a healthy
diet and should be eaten every day? Isn't this belief a part of today's
"Gospel of Good Nutrition"?
It's undeniable that whole grains are good nutrition for some of us.
But it's even more fundamental that there is absolutely no food that is
good for everyone. Who hasn't heard or read the observation made thousands of years ago: "One man's meat is another man's poison"?
Foreword
It's been known for years that certain whole grains [wheat, rye, barley,
spelt, triticale, kamut, and possibly oat) are the cause of celiac disease.
This intestinal-tract disease can vary from mild [gas, bloating, loose
stools) to life threatening (malabsorption, weight loss, malnutrition) and
is preventable/treatable by completely eliminating all of the aforementioned
grains from the diet. But isn't celiac disease rare? Less than one in
one hundred Americans are diagnosed with this problem. Why should
the rest of us worry?
Over the last two to three decades, at an accelerating pace, researchers
have demonstrated that the offending proteins in these cereal grains (including
gluten, gliadin, and glutenins) can cause symptoms, and sometimes
entire diseases, in nearly any area of the body, and not involve the
intestinal tract at all! These problems are often called "non-celiac glutensensitivity symptoms and diseases,""gluten-sensitivity symptoms and diseases,"
or simply "gluten sensitivity." This last term includes, but is not
limited to, celiac disease. It also includes problems caused by sensitivity
to grain subtraction proteins such as gliadin and glutenins.
The scope of the problem is much greater than imagined even a
decade ago. A list of more than one hundred andfifty diseases and symptoms
associated with sensitivity to gluten and other grain proteins, compiled
by prominent researchers, can be found in appendix D of this book.
I first became aware of the wide reach of gluten sensitivity in the
1980s when I read Relatively Speaking, a book first published in Australia
and republished in the United States as Your Family Tree Connection
(unfortunately this classic, basic reading for any health-care practitioner
or serious student of health, is now out of print. It can still be found
through online sources of used books). Written by Dr. Christopher Reading
and Ross iVIeillon, it describes Dr. Reading's detective work in unraveling
the causes of "undiagnosable" symptoms through close examination
of family health history.
When in Australia in the late 1980s, I had occasion to visit Dr. Reading's
office in a suburb of Sydney. On one wall was a chart that would be
amazing to any health-care practitioner even today: a list of over one
hundred individuals who had initially consulted Dr. Reading about what
Foreword
xl
they assumed to be lupus (systemic lupus erythematosus, SLE). When
they first saw Dr. Reading, all had had symptoms (fever, joint pains, and
skin rash are among the most common) and positive blood tests. But
since consulting him, everyone on the list had been symptom free with
negative blood tests for five years or morel That's right: over one hundred
people cured of lupus in the 1980s. Even in the United States of 2002,
any lupus specialist will tell us that's impossible and resume writing prescriptions
for Prednisone, a dangerous, synthetic version of the natural
cortisone molecule.
How did Dr. Reading do it? His program included complete elimination
of all grains from the diet, except rice and corn (it also included elimination
of milk and dairy products combined with heavy nutritional supplementation
both orally and intravenously).
On returning to the United States, I headed tor the university medical
library, where I found a short but very intriguing article in the British
medical journal Lancet. The author pointed out that many autoimmune
diseases shared a common genetic marker called "HLA-B8," much more
commonly than would be expected by chance. The list of HLA-B8 linked
diseases were as follows:
Addison's disease
Autoimmune hemolytic anemia
Lupus erythematosus
(systemic)
Celiac disease
Myasthenia gravis
Childhood asthma
Pernicious anemia
Chronic autoimmune hepatitis
Polymyalgia rheumatica
Dermatitis herpetiformis
Scleroderma
Diabetes mellitus
Sjogren-Larsson syndrome
Graves' disease
Thyrotoxicosis
Insulin-dependent diabetes
Ulcerative colitis
(type 1)
Vitiligo
The author's key point was that every one of these diseases except
celiac disease is autoimmune—diseases thought to be caused by an internal "reaction against self" But celiac disease was known to be caused by
xii
Foreword
an external agent, gluten (which includes gliadin and glutenins as well).
The author asked: Could this external agent, gluten sensitivity, also be involved in causing the rest of these H LA-B8-1 inked diseases?
I thought Dr. Reading had proved this to be the cause in systemic
lupus erythematosus (SLE) by helping over one hundred people to
cure their "lupus" by (among other things) totally eliminating all glutencontaining grains from their diets. So, since the 1980s, every time anyone
consults me for any of these conditions, I recommend absolute avoidance
of all gluten-containing grains (I also recommend absolute avoidance of
milk and dairy, comprehensive allergy testing and desensitization, gastric
analysis, large quantities of omega-3 essential fatty acids, many oral and
intravenous vitamin and mineral supplementations, and testing and treatment with DHEA and testosterone. A complete explanation isn't possible here.)
The results have been fantastic (compared to "conventional treatment," which usually consists of Prednisone prescriptions and other
immune-system-destroying patent medicines). Although not everyone
has been cured of these HLA-B8-linked diseases, a very high percentage
of them have had major improvement or complete remission. The exception has been established type 1 diabetes, where already-destroyed
islet cells cannot be brought back to life, even by a gluten-free diet, and
insulin treatment needs to be continued. But without permanent glutengrain elimination, the rest of the program won't work nearly as well for
any of these problems.
This book has reminded me that gluten sensitivity not only extends
far beyond celiac disease and the HI,A-B8-linked autoimmune diseases
listed above. Dr. Braly and Mr. Hoggan estimate that 90 million Americans may have non-celiac gluten sensitivity. They write that undiagnosed
sensitivity to gluten, gliadin, and other grain proteins is
the root cause of many cancers, autoimmune diseases, neurological
diseases, chronic pain syndromes, psychiatric and other brain disorders, and premature death. There is also a clear causal connection with some cases of osteoporosis, epilepsy, learning disorders,
Foreword
xiii
attention deficit disorders, infertility, miscarriage, premature births,
chronic liver disease, and short stature.
They also include complete lists of other gluten sensitivity-linked symptoms and diseases. Although written well for any of us to read, this book
carefully includes 383 citations for health-care professionals and serious
students.
Dr. Braly is a longtime clinical investigator into allergy, sensitivity, and
health. He emphasizes that anyone who has gluten sensitivity also has
other food sensitivities, and frequently many of them. I completely agree
with his view that gluten/gliadin/glutenin sensitivities (along with milk/
dairy sensitivity) are often "basic" or "root" sensitivities, which then lead
to the development of many other allergies and sensitivities. When gluten
sensitivity (or milk/dairy sensitivity) is found, comprehensive allergy testing should always be done. But even though desensitization techniques
can successfully eliminate other allergies and sensitivities, no one should
try to desensitize gluten/gliadin/glutenin sensitivities in order to stay well.
They should be permanently eliminated from the diet of anyone who has
a sensitivity to them.
Remember, gluten sensitivity includes but is not limited to celiac disease. While the "gold standard" for measuring celiac disease was an intestinal tissue biopsy, followed by gauging any characteristic changes in the
biopsied tissue, many gluten sensitivity-linked symptoms and diseases
listed in Dangerous Grains are not accompanied by changes in the intestine. Unfortunately, medicine as conventionally practiced doesn't accept
this research-documented fact yet, even though it was first found to be
the case by conventional practitioners years ago in the disease "dermatitis
herpetiformis" (another HLA-B8-linked disease). Even though intestinal
biopsies are often normal in dermatitis herpetiformis sufferers, the problem always clears up completely with strict gluten-grain elimination.
Fortunately, the development of highly accurate blood tests for gluten
sensitivity has made diagnosis much easier and has greatly facilitated research. Before briefly mentioning the blood tests (which are detailed much
better in the pages that follow), remember that Dr. Chris Reading figured
xiv
Foreword
out many of the disease and symptom connections with gluten sensitivity
by examining family trees for various symptoms and diseases. Armed with
a copy of Dangerous Grams for a comprehensive list of illnesses and symptoms, we can then do our own family trees of medical history and make
an educated guess about whether we are at risk for a gluten-sensitivity
problem.
The most sensitive and specific blood test for gluten/gliadin sensitivity presently available is the "tissue transglutaminase" (tTGj, It's the test
I've used since it became available in 1999. Others include "endomysial
antibodies" (EM A), which check mostly "short-lived" antibodies, and "antigliadin antibodies" (AGA), which check "longer-lived" IgG antibodies as
well as IgA antibodies.
Very important: We don't have antibodies to anything unless we've
been exposed to it! If you've been avoiding all "gluten grains," the test will
be negative even if you're truly gluten sensitive.
W H Y SHOULD GRAINS BE
SUCH A PROBLEM?
As previously noted, bread made from grains has been called the "Staff
of Life." But research shows that agriculture and grain farming have existed at most for ten to fifteen thousand years, and humanity has been
on this planet for much longer than that. For over 2 million years, our
remote hunter-gatherer ancestors ate absolutely no grains at all! Agriculture and grain-eating have been around for A
' percent or less of the
history of humanity, and many of us still haven't adapted to grains, especially gluten-containing grains (corn and rice cause their own set of
problems).
This isn't "just a theory." Archeologists and other researchers have
found that gluten-grain eating originated in the Middle East (Mesopotamia)
and spread westward to the Mediterranean basin and northward into
Europe. Since gluten sensitivity can cause or contribute to infertility, re-
Foreword
current spontaneous miscarriage, amenorrhea (no menstrual periods),
and low birth weight, there should be less surviving individuals with the
HLA-B8 genetic characteristic in the areas first (and therefore longest)
exposed to gluten-gliadin grains. This is, in fact, the case: The highest
percentage of individuals who still have HLA-B8 (and other gluten sensitivity) genetic markers is found in the areas of Europe furthest away from
the original source of gluten grains.
If we remain ignorant of the gluten grain-human genetic misfit (remember, this misfit doesn't occur in all of us, just a large percentage), it'll
still be much longer than another ten thousand years before consumption
of gluten grains removes all of us sensitive to them from the gene pool. In
the meantime, there'll be a lot more illnesses, suffering, and premature
death than we need to have, even given present knowledge.
If you have any suspicion that gluten grains may be contributing to
your symptoms or illness, read the rest of this book! Then check with a
health-care practitioner skilled and knowledgeable in both nutritional
medicine and allergies. Such a practitioner is very like to be a member of
the American College for Advancement in Medicine (ACAM, 1-800-5323688, www.acam.org), the American Academy of Environmental Medicine
(AAEM, 1-316-684-5500, www.aaem.com), or the American Association
of Naturopathic Physicians (AANP, www.naturopathic.org). However,
make sure to take a copy of this book with you to loan to the doctor (unless the doctor is Dr. Braly) because he or she will likely learn a lot from
it, as I did.
If you find you have a symptom or disease related to gluten sensitivity, and you feel better after eliminating gluten-containing grains from
your diet (along with other food allergies and sensitivities), give a copy
of this book to a relative. Remember, Dr. Reading "figured it all out"
without intestinal biopsies or blood tests, just by a careful examination of
family trees.
Your Family Tree Connection first brought the public useful information about the health hazards (for many of us) of gluten-containing
grains. In Dangerous Grains, James Braly and Ron Hoggan have given us a
xvi
Foreword
very much needed, and expanded, and updated picture of the health
problems associated with gluten-containing grains—health problems affecting so many, but known by so few.
Jonathan V. Wright, M.D.
Medical Director, Tahoma Clinic
Kent, Washington
Author:
Why Stomach Acid Is Good for You (2001, with Lane Lenard, Ph.D.)
Maximize Your Vitality and Potency (1999, with Lane Lenard, Ph.D.)
The Patient's Book of Natural Therapy (1999, with Alan R. Gaby,
M.D.)
Natural Hormone Replacement for Women Over 45 (1997, with John
Morgen thaler)
Nutrition
Healing Newsletter (1-800-851-7100, www.tahoma-
clinic.com)
PREFACE
Our personal backgrounds and family histories provide powerful evidence of the hazards of eating gluten, as well as for the subtlety and variability of its devastating impact on human health. Our research was
motivated by our own journeys along the path to wellness and by the
health problems experienced by members of our families.
RON HOGGAN, M.A.
For years I was unaware of the cause of my discomfort. I just assumed
that others were just as uncomfortable. I had variously been called emotional, picky, fussy, attention seeking, and a hypochondriac. I was diagnosed with an ulcer, a colicky appendix, and irreversible neurological
damage related to a partial hearing loss. I also had a long history of
chronic back and leg pain, which I attributed to injuries and aging. I ac-
Preface
cepted my hand tremors and chronic heartburn as reflections of my nervous nature.
All of those difficulties reached a low point on a December morning
in 1994 when I was diagnosed with celiac disease. A fiber-optic tube,
called an endoscope, was inserted in my mouth, down my throat, through
my stomach, and into the upper part of my small intestine. With this device, tissue samples were taken to look for cancer. Thankfully, there was
no evidence of malignancy. While the doctor would have to wait for a
pathologist's report to confirm his suspicions, he was fairly confident that
I had celiac disease and that I should begin to follow a strict gluten-free
diet for the rest of my life.
By eliminating wheat, rye, oats, and barley from my diet, my world became a better place. More than seven years later, 1 now feel whole and
healthy. Chronic pain from a knee injury of more than a decade before
my diagnosis gradually faded away. Untreated, my celiac disease apparently interfered with its healing. Prior to diagnosis, 1 sometimes needed a
cane to get around. Now the cane is collecting dust in the cellar. My vision and hearing improved. 1 experience fewer headaches and less back
pain. The frequency and severity of acid indigestion are reduced. I no
longer feel cold all the time.
After eliminating gluten grains, I realized how uncomfortable and
chronically ill I had been for most of my life. My newfound wellness began my search for the tools to maintain and further improve my health. I
have learned that such multiple, chronic medical conditions that often
do not respond to conventional treatments are characteristic of glutensensitive and food-allergic individuals.
As a part of my journey to wellness, I underwent testing for common
food allergies at the laboratory where Dr. Braly, my co-author, was medical
director. The procedure, called IgG EUSA blood testing, led to further
limitations on my diet. Although these restrictions were quite difficult in
the beginning, I now consider myself very fortunate—most people with
celiac disease are never diagnosed.
Despite considerable research indicating a frightening cancer risk
among those with untreated celiac disease, and recent reports indicating
Preface
xix
that close to 1 percent of the apparently healthy U.S. population is affected by this disease, it is often considered rare and somewhat trivial by
most of today's health professionals. Such perceptions are dangerously
out of touch with the professional literature. I believe that my brother
paid for these outdated beliefs with his life. 1 was to learn that all firstdegree family members are also at high risk for this potentially fatal, genetically driven disease. As soon as I was diagnosed with it, my brother,
mother, and children should have been invited for testing.
Sadly, this was not done. Instead, about ten months after my diagnosis, my brother, Jack, was diagnosed with non-Hodgkin's lymphoma. The
largest, and what was presumed to be the primary tumor, was located
near his kidney.
Despite considerable negotiation, including my brother's and my
repeated requests, the attending physicians resisted testing for celiac disease on the basis that the tumor was not in the intestine and that his lymphoma was the first concern. No diagnostic testing was ever conducted.
My brother died on November 18, 1996. His lymphoma may have been
the result of untreated celiac disease. If so, he might have recovered, as
other patients have, with a combination of conventional cancer treatments and an appropriate diet. Because of the general ignorance of celiac
disease and its role in many types of lymphoma, my brother did not pursue a gluten-free diet to aid his battle against cancer. He was foolishly and
incorrectly told that the diet is nutritionally inadequate and would compromise his chances of recovery.
My Daughter
When Kyra was twenty-four she visited the same specialist that diagnosed my celiac disease. He conducted an endoscopy to take tissue samples from her intestinal wall. The pathologist, another specialist who
examines such biopsies under a microscope, noted a thickening of the
bowel wall. Despite a large volume of research indicating that such a
thickening is consistent with, and usually indicative of, celiac disease, that
diagnosis was ruled out because more dramatic damage was not found.
xx
Preface
A second opinion led to a diagnosis of celiac disease, but not before
Kyra had suffered many more months of depression, lethargy, and abdominal pain.
Later, she wrote a feature article about her struggles, which appeared
in the Summer 1998 issue of Sully's Limng Without, a magazine devoted
to people with food and chemical sensitivities.
JAMES BRALY, M.D.
As a child I suffered terribly from cow's milk-induced migraine headaches. Since dramatically reducing milk in my diet, I've not had a single
migraine in over forty years. As an adult, when I overindulge in cheese, my
joints and lower back begin to ache. No milk products, no aches or pain.
Years ago, while training for marathons, I would begin the day with a
hearty breakfast that included a cup of regular coffee and whole-wheat or
rye toast. I followed breakfast with afive- to ten-mile run. Almost invariably, when I ate bread with my coffee and then exercised vigorously, I
would break out with extremely itchy hives on my upper back, chest,
neck, face, and scalp, agonizingly lasting for one to two hours. 1 soon discovered that it was the gluten in wheat or rye that triggered the exerciseinduced hives.
Today, if I eat breakfast and drink coffee, but without gluten-containing
wheat or rye bread, no hives occur with exercise. Although not a celiac
yet, I do have a definite gluten sensitivity, which expresses itself when 1
exercise. In addition, if I cheat by eating gluten-rich breads, pancakes,
waffles, or bagels, with or without exercise, my abdomen will often swell
almost immediately. I find myself secretly loosening my belt by one to
two inches in order to breathe. Not surprisingly, without the gluten there
is no bloating. Finally, I've noticed over the years that when overeating
gluten cereals I will invariably experience a nagging, productive cough
that vanishes predictably within a day or two on a gluten-free diet.
Preface
xxi
My son, Zack
From three to six years of age, Zack would complain frequently of
deep, severe bone and muscle pain just above one or both knees, lasting
for hours. The pain was often disturbing enough to prevent him from going to sleep at night. I can recall his mother and me spending many hours
rubbing his legs in an attempt to give him some relief. I was reassured by
his pediatrician that it was merely "growing pains," and he would grow
out of it. Along with the leg pain, like I did as a child, Zack suffered from
frequent, one-sided migraine-like headaches.
Zack was also a very short, small child the first six years of his life: his
height and weight were always in the lowest 1 Oth percentile for his age
group. I suspected that something in his diet was stunting his growth and
intuitively knew that he would not grow out of it until we changed his
diet.
When wheat and other gluten cereals were eliminated from his diet,
the leg pains dramatically vanished and have not returned (unless he
cheats with spaghetti); he began growing rapidly. Within the first two
months on a strict gluten-free diet he grew an astounding two inches. Today his height and weight fall in the upper 50 percent of his age group.
His headaches occur rarely, if at all. Also, his food-induced headaches and
leg pains are now a thing of the past.
So it is our personal experiences, combined with the struggles of our
loved ones, that have led us into areas of research that we would not otherwise have considered. We now find that this research aided us both in
providing sound advice on nutrition and testing to readers who are concerned about their health, and the impact of the modern Western diet.
We have discovered insights that would not have been possible if we
had continued with the pro-gluten bias that was part of our education.
Our research taught us great respect for Dr. Willem K. Dicke, Dr. Theron
Randolph, and Dr. Curtis Dohan, whose heroic works have provided a
foundation for understanding the health hazards of wheat. We have also
xxii
Preface
been privileged to observe the encyclopedic memories of Dr. Loren Cordain and Dr. Michael N. Marsh, who have bridged the gap between theories and practical applications, clearing the path to human wellness. Their
work has helped medical science leap forward in its understanding of celiac
disease and a variety of autoimmune diseases, with special emphasis on
the relationship between gluten, the immune system, insulin-dependent
diabetes, and autoimmune thyroid disease.
Our research has also revealed the source of many, perhaps most,
modern cases of osteoporosis, osteomalacia, and other bone diseases. Over
70 percent of untreated celiacs suffer from thinning of the bones. We
have learned how those who suffer from a variety of highly prevalent gastrointestinal diseases such as canker sores, cancers, irritable bowel syndrome, Crohn's disease, ulcerative colitis, and esophageal reflux, often
benefit from a gluten-free diet.
Our journeys of discovery have now become a joint quest to sound
our warning about the dangers of a gluten-rich diet. We hope you will
continue to listen.
Dangerous Grains
INTRODUCTION
B
y beginning to read this book, you are taking an important step
toward learning to control your health and well-being. Your journey
of discovery begins before human civilization, beyond the origins of human farms and cities some ten thousand years ago. We take you back to
look at prehuman primates. As the exploration progresses, we introduce
you to cutting-edge research dealing with the dietary evidence found in
the bones and teeth of our upright walking hominid ancestors who
roamed the earth more than 2.5 million years ago. We highlight the convergence between modern medical research and archaeology that provides a basis for many of the insights we offer here. Frankly, we continue
to be amazed by what we have learned.
We hope that you will use this knowledge as a springboard to dramatically improve your health and at the same time reduce your risk of
developing many of the ailments caused or worsened by eating certain
gluten grains.
2
Dangerous Grains
Over 600 million metric tons of gluten-rich
wheat are grown and
eaten annually, making it the world's most consumed grain, well ahead of
rice and corn. Yet it is also the grain, along with its gluten cousins, rye and
barley, that puts tens of millions of humans at risk of premature death
and gluten-induced illnesses such as autoimmune diseases, cancers, and
osteoporosis. The dangerous impact of gluten not only bears up health issues here in the United States and Canada but also has profound morbidity and mortality implications for much of the world's wheat-addicted
populations.
In those people who are genetically predisposed to gluten sensitivity,
eating these grains has serious detrimental effects on the body's immune
system. Gluten grains often trigger autoimmune diseases, such as insulindependent diabetes and hypothyroidism, where the immune system, instead of protecting the body, aggressively turns against it, causing chronic,
potentially life-threatening diseases. In addition, gluten grains and dairyproducts contain morphine-like substances that affect behavior, cause
learning difficulties, change emotions and moods, and cause or worsen
neurological diseases. These food-derived drugs even alter how our immune system works and, as a consequence, dramatically increase our risk
of developing many different kinds of cancer.
At the end of this book we provide detailed scientific references segregated by chapters so that if you choose, you can confirm our findings
in recent, carefully scrutinized scientific and medical literature. We have
also drawn information from our own clinical and personal experiences,
including real-life reports from ordinary people who have experienced
many of the symptoms and ailments caused by eating gluten grains,
which, until very recently, have been thought to be universally healthful.
WHAT IS GLUTEN, AND H O W
DOES IT CAUSE DISEASE?
Certain grains frequently eaten by humans can cause our immune systems to pathologically react to specific proteins. These disease-causing
Introduction
proteins are universally found within the seeds or grains of wheat, rye,
barley, spelt, kamut, and triticale. The proteins are loosely called "gluten,"
and the cereal grains containing this gluten protein are collectively called
the "gluten grains."
Gluten is made up of several subfractions or families of proteins. The
scientific name for the most studied of these subfractions is "gliadin."
Gliadin is found in all gluten cereals except for oats. Curiously and tragically, gliadin frequently causes the immune system to react as if it is not
a component of nourishing food, but an invading bug or microbe or,
worse, as though it is indistinguishable from normal organ tissues found
in our bodies. These effects of gluten on the immune system, along with
profound nutritional deficiencies that so often accompany gluten sensitivity, contribute to many modern diseases, which we will be exploring in
this book.
Today, these abnormal immune reactions can easily be identified by
appropriate laboratory and clinical testing. The test results can be used to
help identify your risk of developing full-blown gluten-related diseases.
Testing also identifies causal connections between diseases, symptoms,
and gluten consumption; disease prevention and reversal often follow
from a strict gluten-free diet.
WHAT IS CELIAC DISEASE?
Although medical researchers have known for well over fifty years that
wheat and its near relatives cause celiac disease, most are still working
toward a more complete understanding of this fascinating ailment.
Celiac disease, sometimes referred to as celiac sprue, is a genetically
influenced condition that results from eating gluten. More specifically,
celiac disease is an ailment whereby the inside lining of the small intestine, called the intestinal mucosa, is chronically damaged by gluten proteins and their interaction with the immune system.
As recently as 1990 in Europe, and 1996 in the United States, celiac
disease was erroneously considered quite rare. On this side of the Atlantic,
4
Dangerous Grains
it was thought to affect about 1 in 4,850 Americans and Canadians.
Thanks to innovative new laboratory testing, we now know that celiac disease was, and continues to be, grossly underestimated. More than 2 million Americans and Canadians suffer from this gluten-induced illness.
This is approximately forty times the prevalence we were told less than a
decade ago.
When actively sought, celiac disease is found in 1 in every 111 apparently healthy, symptom-free American ad tilts, making it more than twice as
common as cystic fibrosis, Crohn's disease, and ulcerative colitis combined.
The discovery that celiac disease cannot arise in a person who does
not consume gluten grains was resisted vigorously for a number of years.
The hesitation was likely because this information ran contrary to the
widespread belief that these grains were a healthy food, especially in their
whole-grain forms. The claim that they could cause widespread disease
just didn't make sense. It was not until gluten was objectively shown to
injure intestinal tissues, and a gluten-free diet consistently reversed this
damage, that the discovery was finally, if reluctantly, accepted. That reluctance, as you will soon see, slowed recognition of the many ailments
that can result from untreated celiac disease.
Undiagnosed celiac disease is the root cause of many cancers, autoimmune diseases, neurological diseases, chronic pain syndromes, psychiatric and other brain disorders, and premature death. There is also a clear
causal connection with some cases of osteoporosis, epilepsy, attention
deficit disorders and other learning disorders, infertility, miscarriage, premature births, chronic liver disease, and short stature. When a person is
placed on a strict gluten-free diet, reversal of these conditions frequently
occurs.
Despite these terrible consequences and the promise of ctires, only
one of every forty American celiacs is ever diagnosed and treated. The
current rate of underdiagnosis is partly the result of the confusing, "atypical" array of signs and symptoms and, often, a complete absence of symptoms in the earlier stages of this disease.
Introduction
WHAT IS NON-CELIAC
GLUTEN SENSITIVITY?
Celiac disease is just one subset of gluten sensitivity, a message you will
hear repeated throughout this book.
It is our considered opinion that whenever an individual's immune
system is mounting an abnormal reaction to gluten, with or without symptoms, there is gluten sensitivity. Remember that gluten grains, along with
dairy products, are the most common foods in our diet. If your immune
system is identifying and abnormally reacting to any of the proteins found
in gluten, this food poses a potential threat to your health.
Research into human genes now reveals that non-celiac gluten sensitivity, or immune reactions to gluten, may affect as many as 90 million
Americans. The evidence suggests that these gluten-sensitive individuals
face many of the same hazards associated with untreated celiac disease.
They, too, have likely never suspected the underlying cause of their disease or how easily it could be prevented, halted, and often reversed. Gluten sensitivity is much more common, yet it is sought and diagnosed even
less frequently than celiac disease.
The net result of this alarming rate of undiagnosed celiac disease and
gluten sensitivity is a large population that is chronically ill, unresponsive
to conventional therapies, and often desperately jumping from one doctor to another without relief.
To further confound the issue, untreated celiacs suffer a greater risk of
infectious disease, and some evidence suggests a similar dynamic in nonceliac gluten sensitivity. Hence, even where antibiotics provide symptom
relief, there may be an underlying, silent case of celiac disease or nonceliac gluten sensitivity that is increasing susceptibility to opportunistic
infections. An excellent example of this dynamic is recurring middle-ear
disease in children and infants, many of whom are gluten and dairy sensitive. More antibiotics are prescribed to treat the fever and pain, but the
fundamental cause, food sensitivity, is never addressed.
The popular media and conventional nutritional wisdom, including
6
Dangerous Grains
the medical profession's traditional approach to nutrition, have created
and continue to perpetuate this problem through inadequate, outdated
dietary- counseling. Attempts to universalize dietary therapies so that onediet-fits-all influences the flawed claims against meats and fats, thereby
encouraging overconsumption of grains.
Government-sponsored guides to healthy eating, such as the USDA's
food pyramid, which advocates six to eleven servings of grains daily for
everyone, lag far behind current research and continue to preach dangerously old-fashioned ideas. Because the USDA's function is largely the promotion of agriculture and agricultural products, there is a clear conflict of
interest inherent in any USDA claim of healthful benefits arising from any
agricultural product. Popular beliefs and politically motivated promotion,
not science, continue to dictate dietary recommendations, leading to debilitating and deadly diseases that are wholly or partly preventable.
CELIACS TODAY SHOW
DIFFERENT SYMPTOMS
To further confound this highly controversial political issue, authorities
are reporting a fundamental shift in the presenting symptoms of celiac disease. Previously, it was a universal truth that all celiacs present in predictable ways with weight loss, muscle wasting, failure to thrive, chronic
diarrhea, smelly stools, abdominal bloating and cramping, and perhaps
iron-deficiency anemia. Today's celiac displays quite different symptoms,
such as psychological depression, intestinal cancer, insulin-de pen dent diabetes, osteoporosis, short stature, canker sores, and/or chronic liver disease
of unknown cause, to name just a few, In fact, well over 150 medical conditions have now been reported as overrepresented among gluten-sensitive
individuals. (See appendix D for an extensive list of these conditions.)
A misconception also exists that celiacs are undernourished or emaciated. Yet, more of today's untreated celiacs are reported to he overweight
or obese rather than underweight or wasted. The same research shows
that the majority of untreated celiacs are well within the normal weight
Introduction
range. Contrary to prior beliefs, many research papers are reporting that
most untreated celiacs have no abdominal symptoms at all.
Whatever health problems concern you, whether for a loved one or
yourself, the answer is often found in diet and how the body reacts to
foods. And the culprit may be the grain products you are eating and enjoying every day. The very food that provided the foundation of today's
civilization, the food that is enshrined in the holy scriptures of several of
the world's oldest religions, the food that is touted as the "staff of life," is
reaily an unexpectedly common, serious threat to human wellness and
existence. Yet even in industrialized countries, these grains serve as humanity's bulwark against starvation.
This is the extremely complex problem we face. Many people eat
grains daily because they are cheap and abundant, yet science is reporting
that these very same grains are bringing us to the brink of an enormous
health crisis.
It is doubtful that the earliest farmers ten thousand years ago were
aware of the health implications of the shift to gluten grains as a dietary
staple. Even with today's sophisticated medical laboratory technologies
and protocols, the health hazards of gluten-containing grains are being
recognized by only a handful of medical researchers. This is due to absent
or nonspecific symptoms early in the disease process and human bias
rooted in history and psychology, accompanied by a universal reluctance
to embrace radically new information. Acceptance of new ideas is often
coupled with recognition of having been fundamentally wrong all along—
a difficult admission for anyone.
MALADAPTATION TO A SILENT,
DEADLY DISEASE
One may reasonably ask: If the symptoms of non-celiac gluten sensitivity
and celiac disease can be absent, nonspecific, or minor well into adulthood, why is gluten considered a serious health threat to the gluten sensitive? Hans Selye, the father of stress research, answered that question
8
Dangerous Grains
very well in 1936. His discovery and description of the general adaptation
syndrome, following his experiments with animals, offer a clear explanation of this dynamic.
Today, people adapt to eating gluten at a very early age. When first exposed to small amounts of gluten in cookies, crackers, soups, etc., some infants will become ill. If short lived, a gluten-induced illness is likely to be
dismissed as one of the many normal cases of sniffles, colic, or diarrhea
that occurs often during infancy. The connection between illness and eating gluten is rarely made, and infants, as a consequence, will continue to
be fed a certain amount of gluten on most days. What is confusing is that
they soon give the appearance of full recovery. However, if their illness
was caused by gluten, they have only temporarily recovered from the
symptoms but not from the cause of those symptoms—-gluten sensitization. They have simply adapted, or maladapted, to this chronic source
of dietary stress. Regular, frequent consumption of gluten, which is standard dietary practice in most households, maintains and perpetuates this
maladaptation. The term used to describe this dynamic of adaptation to
stress is "tolerance."
It is by means of such a tolerance that many gluten-sensitive individuals, despite their apparent state of good health, will develop a host
of problems that appears to spring from nowhere. Some will develop
short stature, bed-wetting, sleep disorders, headaches, or chronic fatigue,
often accompanied by anemia. Others will suffer chronically from a
vague unwellness, usually without a specific diagnosis, and rarely respond
to conventional medical therapies. Still others will develop one or more
autoimmune diseases, such as thyroiditis, chronic liver disease, or insulindependent diabetes. A small minority will suffer from deadly diseases, to
which they appear to have little normal resistance and die at an early age.
The majority of gluten-sensitive individuals will present a picture of apparently good to excellent health until the fateful arrival of an initial,
often chronic illness. The sufferer will rarely, if ever, be aware of the underlying cause of this ailment.
Undiagnosed and untreated, many gluten-sensitive individuals continue to fall by the wayside as their diet depletes their nutritional status
Introduction
and immune systems, paving the way for the illness that besets them.
Although it would be better to catch this insidious problem in infancy
where it originates, it can be amazingly helpful to catch and treat this dietary condition at almost any age or stage of the disease. Even patients
with advanced stages of cancer and AIDS are reported to improve when
consuming a gluten-free diet.
An Australian psychiatrist, Dr. Chris Reading, has published accounts
of a number of cancer patients battling clinical depression, which he
treated with a gluten-free diet. The diet, in conjunction with conventional cancer treatments, resulted in a full recovery from the cancers in
five out of six patients. Although this publication was not subjected to
the scrutiny of the peer review process, the results are certainly consistent
with that literature and our perspective.
SLOW ACCEPTANCE AND
IMPLEMENTATION OF
N E W KNOWLEDGE
Not only is the publication and dissemination of new knowledge painfully slow, most health professionals are slow to adopt new ideas from
current research. This results in lengthy delays in the application of research to treatment, with patients suffering needlessly and dying prematurely in the interim.
There are a number of reasons for this unfortunate situation. Medical
practitioners are often so overworked that many of them simply do not
have the time to keep up to date on major medical breakthroughs. Even
when doctors can devote some part of their busy days to studying current
literature, it is literally impossible for one to keep up with the tens of
thousands of international articles published monthly. For example, there
are between ten and twenty thousand medical journals and newsletters
published annually. The busy doctor must therefore prioritize which articles he will study. Predictably, most journals and reports will be set aside
and never read. Studies dealing with the health hazards of grains will al-
10
Dangerous Grains
most always be among those that are ignored. Many will see such articles
as highly specialized, esoteric, and impractical. Physicians' prior training,
often a decade or two behind the times, will have created the bias that
gluten sensitivity is a trivial, rare aberration. Following the old adage
"common diseases occur most commonly," most practitioners will choose
to devote their time to studies and diseases that they believe are more
likely to benefit a greater number of their patients. Hence, gluten sensitivity and celiac disease have been disregarded as irrelevant.
How This Book Can Help You and Your Doctor
e realize that most busy physicians will be unable to take
time to look at yet "another health book" brought to them
by a patient who might be considered one of the "worried well" or
"grasping at straws." Here are some suggestions to help you overcome this potential problem. First, find the sections of this book
that are pertinent to your own medical conditions, including those
dealing with laboratory and clinical diagnosis. Next, to help your
doctor gain confidence that the book's contents and your requests
are science-based, look up the relevant citations at the back of the
book under each chapter's list of sources. Prom that list choose
several key articles, preferably with the most recent publication
dates. Go to your local library with the list of sources and order or
retrieve and photocopy the complete articles. When you have all
the articles in hand, take them along when you visit your doctor.
This science-based approach should increase the likelihood of your
physician's confidence and cooperation for several reasons:
1. It will be obvious that you have already invested considerable
time in exploring your health concerns and suspicions.
Introduction
II
2. Because of their training, medical doctors are familiar with
the rigors of the peer review publication process. Your doctor
is much more likely to value this kind of literature.
3. If only because of issues of liability, your doctor will be less
likely to dismiss researchers from many different medical
centers around the world, reporting on carefully controlled
experiments and data analysts.
With the peer-reviewed literature in your hand, you should
feel comfortable asking your doctor to order the relevant laboratory testing identified in this book. With a little extra time and effort you can place yourself back in charge of your own health.
Persistent but out-of-date definitions of celiac disease formulated from
the limited understanding of many years ago also contribute to a delayed
acceptance of new information. Verified technical advances should lead
to rapid redefinition, but too often they do not. For example, celiac disease was first described in 1888 by Dr. Samuel Gee, and reiterated by Dr.
R. A. Gibbons. Their century-old view that celiac disease is solely a disease of malabsorption persists today. In 1888, celiac patients were identified by a failure to thrive and pale-colored, smelly, floating stools. Such
stools, often in association with diarrhea, indicate a high-fat content, so
these children were correctly perceived as malabsorbing dietary fat. Their
description of the disease was limited to their understanding.
More recent advances clearly show poor absorption of essential vitamins and minerals among untreated celiacs, along with many other signs
and symptoms throughout the body. However, the persistent notion of
malabsorption in celiac disease has been overgeneralized and overemphasized, suggesting a general failure to absorb nutrients as the sole or
primary defect. This conception of celiac disease is probably a defensible
understanding of very advanced cases, but it ignores the majority who are
12
Dangerous Grains
either of normal weight or sometimes obese. Carbohydrate absorption
often continues fairly normally.
As a consequence, an out-of-date definition has retarded research into
celiac disease for over a century.
INTESTINAL BIOPSY AND
REDEFINITION
The next step toward a better understanding of celiac disease resulted
from Dr. Dicke's discovery in the 1930s that a wheat-free diet resulted in
a full remission of symptoms. However, the acceptance of this radical discovery was slow, not garnering much attention until around 1950, when
a surgical device was developed to biopsy tiny tissue samples from the
small intestinal lining, It was this invention that belatedly led to redefining celiac disease during the 1960s. Thirty years after Dicke's discovery
and eighty years after Dr. Gee's observations, celiac disease was still being
considered a disease of malabsorption, but it was redefined to exclude
other non-gluten diseases that cause fatty stools and failure to thrive. The
new definition required intestinal damage, verified by a biopsy, which improves after excluding gluten.
This new definition relied on taking multiple intestinal biopsies on at
least two separate occasions. These tiny tissue biopsy samples revealed a
characteristic damage to the intestinal lining in patients with celiac disease. If the second biopsy, taken months later after beginning a glutenfree diet, showed that this intestinal damage decreased or disappeared, a
confident diagnosis of celiac disease wras made. The many other symptoms and signs of celiac disease were also dramatically reduced or eliminated by a gluten-free diet, of course, but curiously this has received less
attention. Even now, the primary focus is on the intestinal biopsy and the
resulting malabsorption.
Absorption of nutrients, especially fats and fat-soluble vitamins, is
compromised by the simple reduction of absorptive surfaces in a damaged intestinal lining. As a consequence, malabsorption has continued to
Introduction
be identified as the primary feature of celiac disease; this is often thought
to explain most, if not all, of its symptoms and signs. Again, this incomplete perception has led to the erroneous conclusion that patients with
celiac disease must, by definition, be skinny, pale, overtly undernourished,
and with a plethora of abdominal symptoms. This unfortunate bias places
many patients at unnecessary risk.
N E W LAB TESTS, N E W DEFINITIONS,
N E W HOPE
During the intervening period of sixty-five years since Dicke's discovery
andfifty years since the development of tools to collect tissue specimens,
huge strides have been made in almost every area of celiac research. Thus,
it is now possible to conduct a rectal challenge with gluten protein in the
doctor's office and get extremely reliable information that would allow
the early and accurate diagnosis of celiac disease.
Highly sensitive and specific laboratory blood tests are more convenient and are already commercially available. They are being routinely used
in Europe and the United States to screen for both gluten sensitivity and
celiac disease. More than any other advancement in celiac disease, these
tests are responsible for the increasing acceptance that gluten sensitivity
is a very common illness, often responsible for an astounding variety of
human diseases. In fact, there is talk in many research circles that, with
some refinements, these screening tests may some day become the final
diagnostic test of choice, entirely replacing intestinal biopsies.
REDEFINING GLUTEN SENSITIVITY
Unfortunately, elements of a century-old definition of celiac disease continue to limit diagnosis to those who show dramatic, advanced damage
to the intestinal wall, representing only a small minority of those with
celiac disease. The large majority of celiacs have silent or nonspecific,
14
Dangerous Grains
non-abdominal symptoms. Those who have specific antibodies against
gluten circulating in their bloodstreams but do not show intestinal damage are frequently ignored, despite serious gluten-induced damage to a
variety of other organs, tissues, and body systems.
For more than a decade now, world-renown od gastroenterologist, celiacdisease investigator, and author Dr. Michael N. Marsh, has been calling for
renaming celiac disease "gluten sensitivity." World-renowned neurological
researcher Dr. M. Hadjivassiliou, as a consequence of observing gluten
sensitization in over half of his chronic neurological patients, has joined
many other gastrointestinal researchers in calling for inclusion of non-celiac
gluten sensitivity. Dr. Hadjivassiliou advocates that all patients with chronic
neurological illnesses of unknown cause be routinely tested for gluten sensitivity. He recommends a gluten-free diet to all gluten-sensitive patients.
The broadened definition that many of these scientists are now advocating also includes routinely testing all patients for certain "genetic markers," such as human leukocyte antigen (HLA.] markers; these are proteins
found on the surface of our white blood cells that help identify susceptibility to dietary gluten.
A TREATMENT IN NEED OF CHANGE
The treatment of celiac disease has changed very little since the 1930s,
with acceptance that wheat and related grains were at the root of celiac
disease. While a strict gluten-free diet remains the only proven means of
controlling this disease, recent research has shown that many celiac patients require a variety of additional tests and treatments to ensure optimum health.
The current unawareness of relevant research among U.S. and Canadian physicians dictates that comparatively few celiacs are ever diagnosed.
Those few who are evaluated properly are usually underweight, complaining of abdominal symptoms, and have consulted a physician who is somewhat knowledgeable about celiac disease. These fortunate few are then
referred to gastroenterologists more current in their knowledge about
Introduction
celiac disease. In turn, the gastroenterologist has the biopsies carefully
examined by a pathologist who is trained to have a high level of suspicion
for celiac disease. For the diagnosis of celiac disease to be made, all three
physicians must be current in their research, recognize the importance of
identifying celiac disease, and ever vigilant.
Given all the pitfalls, it is a bit more understandable why only one out
of every forty of America's celiacs are diagnosed today. Yet it remains an
unacceptable, deplorable situation. If not reversed soon, the continuing
trend of undercliagnosis and delayed treatment may spell disaster for the
American and Canadian health-care systems.
Blood tests for detecting gluten sensitivity and celiac disease and their
dietary treatment impose little burden on our health-care systems. The
cost of diagnosing and treating celiac disease, thereby preventing and
reversing chronic pain syndromes, risk of cancers, osteoporosis, and complications of problem pregnancies, is comparatively cheap. This cost is
significantly less than chemotherapy treatments, surgery to remove a tumor or fix a fractured hip, or long-term treatment of rheumatoid arthritis. More important, the cost in dollars pales next to all the unnecessary
chronic, unremitting human suffering. Clearly, it is to the economic, social,
and moral advantage of medical systems and health consumers everywhere to become aware of and much more vigilant in their search for
celiac disease.
ADEQUATE FOLLOW-UP AND
GUIDANCE BADLY NEEDED
Those diagnosed with celiac disease or gluten sensitivity are usually sent
home with little helpful information. Newly diagnosed celiac patients are
unlikely to be given information about the very high risk of celiac disease
among their immediate family members, even though celiac disease is
largely genetic and is transmitted from one generation to the next. Firstdegree family members are rarely encouraged to be tested and rarely notified of this potential danger to their health.
16
Dangerous Grains
The extreme importance of strict, lifelong compliance with a glutenfree diet and the highly addictive nature of gluten are rarely adequately
addressed. This explains in large part why the reported rate of strict
gluten-free compliance is only about 50 percent.
Celiac patients are also not informed that they may have multiple
delayed-onset food allergies. It is rare, indeed, that a celiac who continues
to experience chronic symptoms after going gluten-free is tested for additional allergic foods. Yet, when celiac patients who remain symptomatic
on a gluten-free diet are tested for additional food allergies, they often report good to excellent relief of symptoms with food allergen elimination.
Thirty-nine out of forty celiacs in the United States and Canada go
undiagnosed. Most of them continue to struggle with ill health, uncertain
about which way to turn, often blaming themselves for their compulsion
to eat, chronic discomfort, lethargy, and fatigue. Many feel, after consulting with their doctors, that they have been summarily and abruptly dismissed with a symptom-chasing prescription drug or with reassurances
implying in so many words that their problem is "all in their heads." Undetected celiacs die twice as frequently as non-celiacs, usually from cancers, but also osteoporotic hip fractures or complications of autoimmune
diseases. Others endure avoidable, treatable chronic pain and disability.
Learning to recognize gluten as a common underlying cause of many ills
offers a sane, science-derived alternative explanation, giving hope to millions with chronic pain, that it is not their fault and that they can, at last,
find permanent relief by dealing with the cause.
As you will learn in the following chapters, few of us really need tranquilizers, sleeping pills, antibiotics, hormone replacement, nonsteroidal
anti-inflammatory drugs, or other pain-reducing medications to mask symptoms or our awareness of those symptoms. Instead, we need an effective,
scientific, cause-oriented alternative to symptom-masking therapies. Many
of you will find that alternative in a gluten-free diet.
When you finish reading this book, you will have a much better understanding of the dynamics that may be causing your disease, and indicators of potential, but preventable health problems that can result from
consumption of grains.
Introduction
The plague of the twentieth century was not cancer. Neither was it
heart disease. Last century's plague was an insidious one that should have
been recognized and treated long ago but wasn't, This plague remains
poised, ready to harm many unwary victims. The signs of this growing,
worldwide epidemic are apparent everywhere, to the initiated, including
those who choose to read and carefully study this book. The worldwide
epidemic is the plague of gluten gluttony, an overconsumption of wheat,
rye, barley, and other gluten cereals by the vulnerable, genetically predisposed.
It is the explicit and recurring theme of this book that eating gluten
grains drives much of mankind's chronic illness and that our escalating
consumption of these grains is countering the many medical advances
that are working to extend our lives. Through understanding the dynamics by which this occurs, our readers will be powerfully armed to protect
themselves and their loved ones.
1
Grains and People:
An Evolutionary Mismatch
PLEASE N O T E :
Although we draw much of our information for this chap-
ter from the European-Middle East experience, this is perhaps evert more
valuable information for Asians, sub-Saharan Africans, Native Americans,
Polynesians, and people of similar racial backgrounds because they have
had significantly less time to adapt to consuming gluten. Europe and the
Middle East are simply the birthplaces of wheat, rye, and barley cultivation, providing us with a rich source of information that has profound,
worldwide relevance.
O u r culture is steeped in pro-grain beliefs. You were probably taught
that grains are a healthy food. T h e y certainly played an important role in
the development of Western civilization. Through religious beliefs, history classes in our schools, and our culinary traditions, grains have been
Grains and People: An Evolutionary Mismatch
19
given our cultural seal of approval in the absence of any scientific investigation. As a culture, we have simply ignored the growing body of evidence against grains, erroneously dismissing this information as applying
only to a very few people or as a trivial concern voiced by hypochondriacs. Yet, there is a persuasive convergence of evidence against grains from
several fields, including medicine, genetics, and archaeology.
In this chapter we offer a very brief exploration of that evidence,
beginning with an archaeological overview of the evolution of preagricultural humans. Then we move to a discussion of the adoption of agriculture. We also provide information about how a leaky gut occurs among
the genetically susceptible, often resulting from eating what is now our
principal food—grains.
NATURAL SELECTION
Nature selects traits that allow individuals to survive long enough to reproduce. It may seem obvious, but if we die before we have children, our
genes will not be passed on. For this reason, genetic diseases that fatally
affect children are likely to decrease over generations. Further, youngsters
are less likely to survive and pass on their genes if their parents do not
survive long enough to help them through those first, most vulnerable
years. Thus, the people whose parents live at least a few years beyond reproduction enjoy a selective advantage.
The impact of eating grains usually occurs well after reproduction, often in middle age. Therefore, the selection process puts only a little pressure on those who are gluten sensitive.
Our Four-Million-Year-Old Gene Pool
Our genetic heritage was shaped by the selection process. At least four
million years ago, our branch of primates, called "upright" hominid, separated from great apes, gorillas, and chimpanzees. They have continued to
evolve along their own branches of the primate tree, yet we continue to
20
Dangerous Grains
share more than 98 percent of our genetic heritage with the chimpanzee.
This suggests just how slowly genetic change occurs in complex animals,
such as humans, who must typically survive more than a decade before
reproducing.
The diet of our closest genetic relative, the chimpanzee, supports the
perspective that fruits and vegetables are healthful. It would be a mistake, however, to adopt a vegetarian perspective based on that rationale.
Chimps do eat a great deal of fruit—when they are not eating each other!
Recent observations suggest that cannibalism among chimpanzees is fairly
common. Today's chimpanzee also hunts, kills, and eats small mammals.
In fact, meat constitutes about 15 percent of the chimpanzee's diet. The
notion that our evolutionary roots are strictly vegetarian is seriously flawed,
even when viewed through the distorted lens of the contemporary chimpanzee's diet. The lesson, however, is an important one. Consumption of
animal flesh has long played a significant role in the genetic past of our
species.
Selective Advantage
In every species, the survival value of genetic mutations is constantly
being tested by nature. Those new traits that continue from one generation to the next usually reflect an improved adaptation to the environment. Since the time we developed omnivorous teeth that functioned
well for eating both vegetables and animals, our evolutionary heritage
shifted to a greater general reliance on meat and internal organs. The human species and its forerunners survived, thrived, and evolved eating fish,
meat, organs, vegetables, and fruit, for at least 1 million, and probably
about 2.5 million years. Yet, humans have only been eating grains for the
last twelve thousand years, showing the brevity of the span of evolutionary time during which we have been consuming grains. This means that
humans have been eating meats and other animal parts 207 times longer
than we have been eating grains. In other words, grain consumption has
only taken place for less than one half of 1 percent of our evolutionary
history.
Grains and People: An Evolutionary Mismatch
21
Further, it is only those populations descended from the early farmers of the Middle East and southern Europe that have been eating significant quantities of cereal grains for as long as twelve thousand years.
Most of the world's populations have had much less time to adapt to
this very new food. Some groups of humans, including most aboriginal
peoples throughout the world (such as Australian Aborigines and Native
Americans) have had only a few centuries of exposure to gluten grains.
In simplest terms, adaptation requires that only a minority of members
of a particular species enjoys a selective advantage. The rest are culled
from the gene pool. Adaptation is a ruthless process that can visit considerable suffering as it selects the most suitable genes for the current
environment.
The 1993 Nobel Prize winner in chemistry, Kary Mullis, says that the
"DNA molecules in our cells are our history." It is this genetic history that
has shaped us. Our immune sensitivities and our nutritional requirements are decreed by the millions of years during which nature shaped
our genes, our biochemistry, and our bodies. It did so through the interaction between the food in our environment and our ability to use it for
energy, growth, and health. Thus, available foods shaped our genes, and
our genes shaped our dietary requirements.
Modern humans were tall and robust when they spread through
Africa, Europe, and Asia about forty thousand years ago. Like the Neanderthals and homo erectus before them, until the appearance of agriculture, the diet of modern humans was dominated by animal proteins and
fats. There is considerable debate about the time at which we began to
use cooking fires, with estimates ranging from two hundred thousand
years ago tofifty thousand years ago.
By the time we started cooking our food, meat and internal organs already formed a major part of our diet. Our hunter-gatherer ancestors
rarely, if ever, ate wild cereal grains prior to about 15,000 B.C. These grass
seeds were very hard and could not provide any significant nutrition if
eaten without grinding and cooking. Further, gluten grains, which are late
arrivals to the human diet, lack many of the nutrients we need. They also
contain substances that are harmful to us. These facts of grain composi-
22
Dangerous Grains
tion clearly demonstrate both the short time we have been consuming
them in any quantity and the poor suitability of grains as a dominant source
of nutrients,
HUNTER-GATHERERS
We know that throughout most of recorded history humans usually lived
short, difficult lives replete with famine, pestilence, and a high infantmortality rate. We sometimes assume that this was also the case for their
preagricultural, prehistoric hunter-gatherer ancestors, yet this is probably
not the case. In fact, the available evidence from studies of modern huntergatherers suggests just the opposite.
Several isolated groups of hunter-gatherers were still in existence during the twentieth century. They had maintained their traditional lifestyle
and were carefully observed by scientists like Vilhjalmur Stefansson. In
addition to enjoying more leisure time than many people living in industrialized nations, such hunter-gatherers often lived long, healthy lives.
There are many reasons to suspect that the same was true of our huntergatherer ancestors.
Prehistoric humans with crude tools may have been easy prey for the
passing carnivore. It does seem likely that some of our distant ancestors
provided large predators with the occasional meal, but the evidence also
suggests that this was probably a two-wray street. However, large, planteating animals like the mammoth, mastodon, bison, and elk were probably more important sources of our ancestors' food, if only because there
was less confusion about who was hunting whom. Small animals, regardless of their feeding preferences, would also be attractive prey for early
humans.
Archaeological evidence suggests that upright hominoids were using
tools and hunting meat as much as 2.5 million years ago. Part of the evidence for these deductions comes from the tools used to butcher animals
and extract their bone marrow. Authorities have attributed changes of
tooth shape in these pre-humans to these dietary advances.
Grains and People: An Evolutionary Mismatch
23
THE SWITCH TO AGRICULTURE—
AND ITS ADVANTAGES
Despite the health consequences of agriculture, it offered many advantages to early farmers. Grains can be stored for lengthy periods and with
minimal technology Although hunter-gatherer groups did store food, few
foods are as amenable to long-term storage as grains. Further, it appears
that humans were forced to seek alternative food sources due to the extinction or reduction of many of the world's large mammals. This dramatic
decline among a host of large mammals occurred between ten thousand
and twenty thousand years ago. Agriculture offered an alternative to the
dwindling meat supply.
Early farmers would also appreciate the sense of physical comfort
caused by these grains. Paradoxically, they provide this comfort through
our inability to fully digest some parts of the grain. Undigested partial
proteins, or peptides, found in gluten cereals have morphine-like properties, becoming potent drugs once they enter the bloodstream. Those who
are at greatest risk from these foods often experience something akin to
addiction due to the pleasant feelings caused by these exorphins, suggesting an origin for the phrase "comfort foods."
Another advantage of agriculture is that it allows people to develop
settled communities, which usually resulted in specialization of labor. More
substantial homes and fortresses were built, providing better protection
from the elements, predators, and aggressive neighbors. Farming also supports more people on a given area land, which confers yet another defensive
advantage. There is little doubt that agriculture offered many attractions
to the earliest farmers.
Adopting agriculture may have provided humans with a storable food
surplus, yet it had many negative genetic health impacts. Many explanations have been offered for this change in health and stature associated
with grain consumption. Some suspect that it was famine and/or disease
that first prompted humans to begin cultivating and eating cereal grains,
blaming these other factors for the decline in health associated with
24
Dangerous Grains
farming. These arguments pale in light of recent medical and scientific
discoveries.
Our agricultural ancestors became smaller, their bones became weaker
and more diseased, and the size of their brains diminished. Human brain
size, based on head circumference, has diminished approximately 11 percent since the advent of agricultural societies. Modern European huntergatherer men and women stood five to six inches taller than farmers of a
few generations later. Only recently, as a result of DNA analysis, has it become evident that the shorter farmers were actually descendants of the
taller hunter-gatherers. There are many archaeological excavations throughout the world that indicate this cereal-associated dynamic, regardless of
when agriculture was begun. Clearly, the nutrient-rich hunter-gatherer
lifestyle is most likely the factor that decreed the five to six inches difference in stature.
If we take celiac disease as a model for other forms of gluten sensitivity, the evidence clearly suggests that eating gluten in increasingly
larger amounts was, in all likelihood, the primary cause of these reductions
in bone health, stature, and brain size experienced by the first farmers.
Diminution of brain size and brain weight has been reported to be overrepresented in untreated older celiacs. Virtually every adult-diagnosed
patient with celiac disease demonstrates significant reductions in bone
density compared with age-equivalent averages. Short stature is another
common feature of untreated celiac disease. Given today's medical evidence, there can now be little doubt that such changes among early farmers were the direct result of eating grains. The evolutionary pressures
began with the first gluten-containing meal. We started trimming a few
members of the gene pool with each succeeding generation of farmers.
GRAINS EVOLVED TOO
The negative impact of grains on early farmers was comparatively reduced
to that of today. Gluten content is much greater in today's grains. That
may be best understood through the forces of evolution that shaped
Grains and People: An Evolutionary Mismatch
25
these grains. Many of the detrimental changes to grains are the result of
human choices or actions, rather than natural selection. This process, although probably unintentional at first, was partly the result of planting
and harvesting practices.
When ripe, the wild cereal seeds would fall off the stalk and seed the
next year's grass. Fully ripened seeds are only briefly available on the stalk
before falling to the ground. The selective gathering of these mature seeds
would be inefficiently time consuming for hungry hunter-gatherers. But due
to the development of modern farming techniques, today's crops ripen
fairly uniformly because of the many centuries of selection that accompany seasonal harvesting.
Rapid genetic change may be induced, whether among humans or
other species, if it bears on reproduction. Such change can be quite rapid
in a plant that reproduces annually and that is specifically selected for
reproduction. In other words, undesirable genetic traits in cereal grains,
such as the grains falling off the stalk prematurely or ripening later than
the others, would be quickly eliminated.
Further spread of agriculture required additional evolutionary change
for successful grain cultivation in harsher climates. The east-west spread
of cereal farming from the Middle East's Fertile Crescent to Southern Europe occurred quite quickly and required little or no genetic change to
grains. This is due to similarities of day length, climate, predators, and diseases at similar latitudes. On the other hand, cultivation in more northerly
latitudes of Europe required some important changes in genetic traits.
Wheat grown further north must ripen during a shorter number of
longer days and must be able to withstand early frost. Northern grains
were also faced with new predators and diseases. Adaptation to more
northerly latitudes is at the root of an important development of this
wheat seed. Gluten is a group of storage proteins. In order for seeds to
germinate, they need nutrients that are contained within the seed. Northern grains must contain relatively more gluten and other storage proteins
as they must make the most of the shorter growing season and germinate
in the more hostile environment.
Wheat, rye, and barley grains, all members of the grass family, contain
26
Dangerous Grains
particular types of nutrients, or storage proteins, which are very difficult
for humans to digest but are ideal for the germinating grain. One group
of these storage proteins is commonly called gliadin, and it is thought to
do most of the damage to human intestines in cases of gluten sensitivity
and celiac disease. Glutenins are another group of storage proteins found
in gluten. Glutenins are thought to be associated with autoimmune skin
diseases and perhaps certain cases of asthma. Digestion of these storage
proteins requires very specific digestive enzymes, which most of us lack.
The combined increase in storage proteins and the absence of the enzymes required to digest them have created a problem that is further escalated by the appeal of these resilient northerly grains.
This increased gluten content associated with northerly cultivation is
highly prized for its baking characteristics. Heat resistance, elasticity, and
malleability due to high gluten content make baked products that are
more attractive to the eye, with a lighter texture. The Canadian Wheat
Marketing Board proudly guarantees and annually delivers millions of
tons of Canadian 1 lard wheat to major food manufacturers, frequently
winning international awards and acclaim for its "superior" quality wheat
with increased gluten content. The very properties that make this grain
more attractive for culinary uses also increase its threat to human health.
It is an unfortunate trend with a very old heritage.
THE SPREAD OF ROMAN GRAIN
Our earliest exposure to grains was in southeastern Europe, where the
gluten content of grain was comparatively small. Agriculture spread fairly
quickly to the west, but movement to the north was slower. Although
agriculture was fairly widespread by the time of the rise of the Roman
Empire, the Romans aided the development of efficient grain cultivation
throughout most of Europe. However, the Romans did not conquer every
area. Parts of Ireland, Scotland, and Finland managed to evade Roman
rule. Many of the people in these areas have been consuming only small
quantities of grains until very recently. For example, in Denmark during
Grains and People: An Evolutionary Mismatch
27
the 1 950s, many Danes considered wheat bread to be a spccial treat due
to the fact that wheat does not grow well in Denmark, North American
natives have had a similarly brief exposure to gluten. Genetic differences
between these groups and those who have had a longer period to adapt
to gluten may identify some of the most threatening elements of grain
consumption.
GENETICS, THE UNIFYING THREAD
The field of genetics has bridged the gaps between various biological
sciences. Similarly, a growing understanding of the interactions between
evolution and food sensitivities offers to unify the study of the diseases of
civilization. Thanks to DNA analysis, we can look back into the distant
past and see where we have come from. This also allows us to better understand some of the dietary practices from our prehistory; the practices
that have shaped our needs and capacities today.
Because gluten sensitivity is often a silent disease in its early stages,
most people who suffer from it have few identifiable symptoms or illnesses until adulthood. Yet, over a lifetime, those with celiac disease are
about twice as likely to die prematurely This increase in deaths is usually
from common complications of celiac disease such as intestinal cancers,
osteoporotic hip fractures, insulin-dependent diabetes, etc. A trait such
as this that reduces the likelihood of survival should be found in fewer
people of each succeeding generation. However, such early deaths usually
occur after reproductive years, therefore passing on the genes that determine gluten sensitivity. It is thus that this trait continues to be passed
from one generation to the next despite the development and increased
reliance on cereal cultivation. Because of the survival disadvantages it imposes, mostly in the areas of infertility and recurring miscarriage, gluten
sensitivity should slowly diminish in numbers over many generations of
exposure to gluten-containing grains, especially when gluten content is
continually on the rise. I lowever, many of us may be unwilling to pay the
price exacted by the slow pace of natural selection. Reverting to a diet
28
Dangerous Grains
free of gluten may be a preferable choice if you are one of those who are
genetically susceptible.
WHAT'S IN YOUR GENES?
The part of the immune system that is unique to each person is made up
of human leukocyte antigens (HLA). HI-A are associated with the progression of infectious diseases and the susceptibility to an incredibly wide
range of chronic, noninfectious diseases, including celiac disease. In commercially available genetic blood tests, these HLA features are identified
in celiac patients by the proteins found on the surface of certain white
blood cells. For example, on the outer surface of some of these white blood
cells, HLA proteins named DQ2 and DQ8 are found in more than 90 and
94 percent of those with celiac disease, respectively. HLA-B8 is also common in celiac disease and is found in about 80 percent of celiac patients.
The appearance of these HLA proteins in the people of a particular
population is a good indicator of the time that a region has been growing
gluten grains. In Europe, HLA-B8 is found in less than 10 percent of the
people living in the area where wheat was first cultivated thousands of
years ago. Yet, it is found in more than 30 percent of the populations
living in the far northwest of Europe, including the west of Ireland, Iceland, and parts of Scandinavia, especially Finland, where wheat cultivation was introduced much later and where historically such crops did not
fare as well.
The genetic trait that confers gluten sensitivity has remained in the
human gene pool for a very long time, causing untold, unnecessary suffering as it continues undetected. In the minority of cases where gluten
does interfere with reproduction, the impact can be heartbreaking and
extremely stressful. For instance, there is a high prevalence of infertility,
regardless of which spouse has celiac disease. If the expectant mother is
an untreated celiac, she is more likely to experience recurring miscarriages, premature births, and low birth weights. Italian obstetricians have
recently found undetected celiac disease to be so common among women
Grains and People: An Evolutionary Mismatch
who have problem pregnancies that they are advocating that all pregnant
women entering their clinics be routinely screened with blood tests.
With today's scientific and archaeological advances, we now know
many of the diseases that accompany the shift to high cereal consumption. Those populations exposed to gluten within the last few centuries
are demonstrating the devastating impact of adoption of these grains into
the human diet. One need only look at the epidemic of diabetes, thyroid
disease, cancer, iron deficiency, malnutrition, and major depression among
many aboriginal groups just recently introduced to a gluten-rich diet to
deduce the horrible impact on genetically naive populations consuming
these cereals. If we are to deal effectively with this health threat, we need
to understand how proteins are digested and the difference this can make.
Making Essential Nutrients Out of Proteins
The building blocks for proteins such as gluten are amino acids. Food
proteins are made up of twenty common amino acids, eight of which are
absolutely essential. They must be found in what we eat because we are
unable to manufacture them from other nutrients. Several more amino
acids are "conditionally essential." Glutamine and arginine, for instance,
are conditionally essential amino acids. During chronic disease or stress,
we need more conditionally essential amino acids than our bodies are
able to manufacture.
All of these different amino acids are bound together in specific sequences, making up protein chains, or polypeptides, frequently composed
of hundreds, sometimes thousands, of separate amino acid molecules.
Digestion of Dietary Protein
Optimal digestion involves disintegration of these large, complex dietary proteins into smaller particles. Sometimes proteins are reduced into
their smallest units of single, free amino acids. Even peptides composed
of two or three amino acids need not be digested further. These small
molecules can easily be transported through the cells of the intestinal
JO
Dangerous Grains
wall, where they are absorbed into the bloodstream as nutrients. Optimally about 70 percent of digested proteins are absorbed as small peptides, while the remaining 30 percent are absorbed as free amino acids.
Usually, the healthy digestive system wastes the undigested and partly digested proteins as fecal matter.
Some bonds between the amino acids that form gluten proteins are
extremely resistant to intestinal digestion, While some individuals produce a liver enzyme capable of digesting gluten, many do not. It is not yet
clear if the presence of these enzymes provides protection from gluten
sensitivity, but it does seem probable. For the many who lack these digestive enzymes, grains need much more processing than the foods that are
common to a hunter-gatherer's diet. Even after grinding, cooking, and the
many assaults of processing and digestion, some of these gluten proteins
remain stubbornly intact. The mucus that lines our intestines usually protects our bloodstream from these stubborn proteins.
Undigested Grain Proteins Spell Trouble
Ideally, we would waste all of these often-indigestible proteins and go
on to our next meal unharmed. However, there is a lot of evidence to
show that somewhere between 15 and 42 percent of the general population are absorbing some of these undigested and partly digested gluten
proteins into their blood by passing them between the cells that line
the intestinal wall. Once in the bloodstream, antibody production often
follows, causing inflammation at the site where these proteins are being
leaked. The chemicals released as a result of inflammation cause even
greater permeability, and a self-perpetuating cycle is established.
This abnormal intestinal permeability, aptly labeled "the leaky gut
syndrome," results from a variety of causes, including gluten sensitivity.
Because gluten proteins have been shown to damage many internal organs and tissues on contact, absorption of these partly digested proteins
is a major threat to one's health even in the absence of specific antibodies against gliadins or other gluten proteins.
Grains and People: An Evolutionary Mismatch
31
Our Tennis-Court-Sized Intestinal Lining
As proteins move along the digestive tract, they come in contact with
the mucosal lining of the small intestine, which serves at least three important functions:
1. It releases many gut hormones and enzymes that stimulate or aid
digestion and intestinal immune function.These hormones also communicate with the brain and heart;
2. It absorbs health-promoting nutrients from food;
3. It acts as a selective barrier, blocking absorption of undigested or
partly digested proteins, as well as toxins, anti-nutrients, bacteria,
yeast, and parasites.
The importance and extent of these three functions is reflected in the
size of the mucosa of a healthy small intestine. If it was spread out and
flattened to show its entire absorptive surface, it would be larger than the
playing surface of a tennis court!
Like the skin, our intestinal lining serves as a protective barrier against
the environment. It has the highest concentration and mass of immune
cells in the entire human body. Unlike the skin, however, the lining is only
one cell thick. These tens of billions of highly specialized cells are replaced
very rapidly, normally about every seventy-two hours. Imagine growing
an entirely new skin every three days—which is just what healthy intestines do. Curiously, this extraordinarily dynamic selective barrier is the
first to be cannibalized and destroyed when we're exposed to any form
of severe stress such as major surgery, radiation, chemotherapy, ultraendurance sports, severe burns, and, in some cases, gluten. Recent research
conducted by Loren Cordain, a researcher at Colorado State University,
has also reported several anti-nutrients, psychoactive substances, and
other non-gluten agents discovered in cereals that can damage the human
intestinal wall.
32
Dangerous Grains
YOU MAY BE ASKING:
WHAT DOES ALL THAT MEAN TO ME?
If you are a member of that large segment of the U.S. population that is
at greater risk of having a leaky gut, or if you undergo one of the many
events that can cause temporary leakage, you are inviting undigested gluten
into your bloodstream. This assumes, of course, that you are eating what
has become a normal diet that includes wheat, rye, and/or barley. Since
our digestive tract is designed to absorb nutrients through the cells in the
intestinal lining, not through gaps between these cells, when absorption
occurs between the cells, the protective function of the intestinal tract is
thwarted.
Under such circumstances, you not only risk absorbing undigested and
partly digested proteins from gluten, tood additives, other dietary proteins, and toxins into your blood, you also increase your risk of infectious
disease. Bacteria that is normally held within the intestine and not associated with infection may be absorbed whole into the blood, depositing in
distant tissue, causing infections and autoimmune reactions. This process
is called "bacterial translocation." Other bacteria, perhaps from the food
supply, may also be allowed access to your bloodstream. Clearly, a wide
range of ailments can develop as the result of a leaky gut.
OUR IMMUNE SYSTEMS
Occasional or chronic leakage of proteins into the blood can take varying
periods of time to produce a wide range of signs and symptoms. It is thus
difficult to identify the cause of many resulting illnesses. Even making the
connection between symptoms and a particular food can be difficult. Delayed reactions to foods, from several hours to several days, are common
and are called "delayed-type hypersensitivity." The delay is caused by the
time needed for these foods to be processed in the stomach, released into
Grains and People: An Evolutionary Mismatch
33
the intestine, absorbed into the circulatory system, and an immune response to be activated. Some elements of the immune system require as
much as seventy-two hours to begin acting against such invaders.
Gluten, if allowed to remain in circulation, while also constantly being replenished by the diet, will cause damage to a variety of tissues and
body organs. Gluten sensitivity has long been seen as an immune system
error. However, gluten will also injure many human tissues. Since it will
cause this tissue damage, whether it gained entry into the blood through
gluten sensitivity or by some other means, an immune reaction to these
proteins may not reflect a flawed immune system. The critical issue appears to be whether gluten gains entry into the blood. Therefore, celiac
disease represents only a small sector of the range of human immune reactions to the presence of gluten either in the intestinal tract or in the
bloodstream because about 15 percent of the population demonstrates
some type of immune reaction to gluten proteins.
The first time the immune system is exposed to a particular foreign
protein, there is a delay before an immune response is fully mounted. Following that first exposure, our immune system will often work rapidly to
seek out and destroy this invader whenever it appears again. This is the
result of memory cells that were developed against that foreign protein
during the first exposure. This occurs whether these proteins are in the
form of a bacterial, fungal, parasitical, or viral infection, or in the form of
an allergen.
Thus, among the genetically susceptible, after the first leakage of
gluten into the blood, every time gluten is present in the intestine, a healthy
immune system identifies the presence of gluten through intestinal sensors, and cascades of immune responses follow. Many researchers exploring gluten sensitivity have expressed the notion that the vigorous immune
response mounted by people with celiac disease probably enjoyed a selective advantage in preagricultural societies. This may be the result of a
form of vaccination.
34
Dangerous Grains
EARLY VACCINATION
Most vaccinations inject dead infectious agents into the bloodstream.
This will sensitize the immune system. The "invader" proteins, although
dead, result in the creation of memory cells, so that the next time these
proteins are detected in the blood, a rapid reaction can be mounted. Such
subsequent reactions are usually so rapid that we often do not develop
any symptoms and are probably unaware of the return of this invader.
A genetic inclination to develop a leaky gut may have served a similar
function among hunter-gatherers. Infants fed small amounts of other foods,
in addition to suckling the mother's milk, would be swallowing many
bacteria. Some of the bacteria from these foods, and some from the breast
and/or hands that fed them, would pass through the stomach and into
the intestine. Although likely to be killed by the acid environment of the
stomach and maternal antibodies in the milk, some proteins would predictably remain intact to be absorbed through the intestinal wall and into
the bloodstream. Here, a very early, effective form of vaccination might
develop.
OUR CHANGING FOOD SUPPLY
Our food supply is narrowing. It is a trend that we have continued since
adopting agriculture, moving away from animal fats and proteins toward
a cereal-dominated diet. Today, few of us consume meat from a wide variety of wild animals. Our diet is restricted to a small variety of domestic
meats. Neither do we liberally choose from over three hundred species of
edible plants. Today, we are restricted to a very small selection of twenty
to thirty vegetables and fruits, and most of us choose from a much narrower range dictated solely by preference. The majority of our calories
and much of our dietary protein come from cereal grains, mostly wheat,
rice, corn (maize), and cow's milk products—-foods never touched by
most humans as recently as just a few thousand years ago. Our genetics
Grains and People: An Evolutionary Mismatch
35
are unchanged, but our diet has been radically transformed, and therein
lies the rub.
Dairy and gluten-grain products combine to make up the top six foods
we now eat. Yet cow's milk and wheat are two of the most commonly reported allergens in the world. With individuals genetically predisposed to
food allergies and gluten sensitivity, eating these same nonancestral, genetically incompatible foods in large quantities day in and day out, is it
any wonder that so many people suffer from chronic food sensitivities?
2
Types of Celiac Disease
and Non-Celiac Gluten Sensitivity
Y
ou may be wondering why it is important to devote an entire chapter to the various types of celiac disease and gluten sensitivity. In
chapter 1, we discussed a number of ways that gluten can affect the body.
Yet, most research attention involving gluten has been focused on only
one expression of gluten sensitivity—celiac disease. Because of the amount
of information that exists about celiac disease, it does provide the best
window through which to examine the broader realm of gluten sensitivity Still, it is important to emphasize that the people with celiac disease
represent only a small portion of the population that is adversely affected
by gluten. Applying assumptions and generalizations about one form of
gluten sensitivity to all gluten-related conditions is potentially dangerous.
In this chapter we offer information that will help you avoid this pitfall
and identify the differing types of gluten sensitivity.
In order to better understand the various types of gluten sensitivity, we
will discuss classic celiac disease, atypical celiac disease, silent or asymptomatic celiac disease, latent celiac disease, non-celiac gluten sensitivity,
Types of Celiac Disease and Non-Celiac Gluten Sensitivity
37
and examples of specific ailments affected by gluten. While these conditions all respond positively to a gluten-free diet, there is great variability in
how they should be managed in addition to compliance with the diet. Each
form of gluten sensitivity has its own unique characteristics, symptoms,
risks, and degrees of response to treatment. Understanding the range of
conditions will reduce the risk of leaping to risky assumptions about your
health. This chapter will also aid in deciding whether or not a strict glutenfree diet is worth a try.
There are also some specific non-celiac ailments, conditions, and treatments that can be helped by a gluten-free diet, although the reasons for its
benefit are not yet well understood. These conditions include intestinal injuries caused by chemical and radiation therapies, AIDS, and food allergies. It is important not to confuse these conditions with celiac disease,
despite the shared feature of clinical improvement on a gluten-free diet.
There is still considerable variability and uncertainty related to nonceliac gluten sensitivity. If only for this reason, it is important that individuals at risk should have enough information to make an informed
decision for themselves. The risks associated with various forms of gluten
sensitivity are not identical to those of untreated celiac disease. However,
we are forced to base many of our deductions on experience and celiacspecific research, beginning with the most commonly recognized form.
CLASSIC CELIAC DISEASE
Classic celiac disease is a condition that will be familiar to most physicians
and other health-care practitioners. A very limited view of celiac disease
develops where understanding is limited to classic celiac presentation. Yet
this form has been extremely popular in teaching centers for the last forty
years or so. Unfortunately, even with its near universal acceptance, when
a patient demonstrates the signs and symptoms of classic celiac disease,
an accurate diagnosis still takes an average of eleven years in the United
States and Canada. It also frequently requires visiting a number of doctors
before it is even suspected. This is in large part due to the outdated notion
38
Dangerous Grains
that celiac disease is quite rare. Celiac disease is sometimes not sought due
to the faulty belief that it is a fairly harmless condition that can reasonably
wait while other more harmful diseases are ruled out.
The patient with classic celiac disease typically arrives at the doctor's
office appearing pale and lethargic; complaining of diarrhea, excessive
gas, and abdominal pain; and showing signs of malnutrition, a low-grade
am a midlife "baby boomer" currently living in New England. As a
very early teen, after 1 had fainted a couple of times, my family
doctor told my parents that I had iron deficiency anemia. Since I
was a teenage girl and just starting to menstruate, the doctor attributed my anemia to excessive blood loss during my menstrual
cycles. Over the next thirty-five years, at least four different doctors diagnosed me with severe iron deficiency anemia of unknown
cause. I managed to increase my iron by taking supplements and
eating high-iron foods, but as soon as I went off supplemental
iron, my anemia recurred.
In the mid-1980s I began to lose weight, going from 125 to under 110 pounds (at a height of five feet, six inches), and I felt
increasingly fatigued. My fatigue and inability to concentrate contributed to my having withdrawn from two doctoral programs.
Since the early 1990s, I complained of increasingly severe lower
back pain, leading to a referral to an endocrinologist, f had developed premature osteoporosis. In the summer of 1997, hip pain
and mobility problems resulted in the diagnosis of a very rare
bone fracture in my right hip. !n the summer of 1997,1 began experiencing intermittent Gl bleeding.
Bv February 1998, with continued GI bleeding, bloating, abdominal pain, and loss of appetite, my primary care physician referred me to a gastroenterologist. By that time, I weighed 90
pounds, and, although 1 didn't know it, 1 had lost over two inches
in height due to osteoporosis. Within ten minutes, after hearing
Types of Celiac Disease and Non-Celiac Gluten Sensitivity
39
my current complaints and medical history-, the gastroenterologist
told me that she was quite certain I had celiac sprue. Her diagnosis was confirmed by both blood tests and a biopsy, f went on a
gluten-free diet. Within three months, blood tests showed that my
iron levels were within normal limits, and, staying on a strict glutenfree diet, 1 have not experienced anemia in nearly three years. My
weight; has also reached a more normal range; 1 have been able to
gain more than 15 pounds and keep it between 108 and 114 most
of the time, except when I'm under stress.
Pat S.
fever, and a bloated stomach, A few pointed questions will soon reveal
that the patient's stools often float and have a particularly unpleasant
odor, suggesting a high-fat content. Although one might expect that such
dramatic signs and symptoms would lead to a rapid diagnosis, this is usually not the case. These classic recognizable manifestations of celiac disease are the exception, not the rule, of celiac patients. Those with atypical
symptoms are very unlikely to get an accurate diagnosis,
ATYPICAL CELIAC DISEASE
Many cases of celiac disease present with a single symptom or with symptoms that are unlikely to be connected with celiac disease. Examples of
such atypical presentations range from life-threatening cavities in the
lung wall to severe cases of rheumatoid arthritis to headaches that just
won't go away. It is a rare practitioner who suspects celiac disease when
faced with such conditions. Yet, there are many dozens of examples of
such atypical symptoms. In fact, we have identified well over 150 medical
conditions and symptoms, most of which should be categorized as atypical celiac disease. A listing is provided in appendix D.
The further one looks into medical literature, the more difficult it be-
40
Dangerous Grains
comes to ignore the possibility of celiac disease in association with almost
any condition or symptom. Celiac disease simply cannot be ruled out without testing, and those who do not suspect, do not test. Even those who
have a high level of suspicion of celiac disease will be misled if they rely
on classical symptoms to suggest celiac disease.
SILENT OR ASYMPTOMATIC
CELIAC DISEASE
Any search for celiac disease based on the presence of symptoms will
miss most cases. This is because nearly half are clinically silent. Over half
of all biopsy-proven celiacs have no abdominal symptoms at the time of
diagnosis, even though intestinal damage has been occurring for years.
One might argue that if the patient has no symptoms, the patient
should be left alone until aggravating symptoms develop. Tragically, as
discussed in hundreds of medical journals, the first, most common presenting symptom of silent celiac disease may be cancer. There is a similarly
grave risk of developing other chronic, potentially life-shortening ailments
that so often follow undetected, untreated celiac disease. For this majority of celiac victims, blood testing is their best, perhaps their only hope
for diagnosis. But this risk can be reversible if a gluten-free diet is begun
early enough. The risk of malignancy may actually be greater among
silent celiacs because so few of them are likely to be diagnosed and hence
have not had the opportunity to reduce their astronomically high cancer
risk through a gluten-free diet.
LATENT CELIAC DISEASE
There are many cases in which celiac disease is suspected but no intestinal damage can be found; yet, months or years later, frank celiac disease
is found. One commonly sees this with first-degree family members of
celiacs and in recently diagnosed insulin-dependent diabetics. The initial
Types of Celiac Disease and Non-Celiac Gluten Sensitivity
41
biopsy is negative, only to turn positive six months to three years later.
This latency and dormancy demonstrate a phenomenon that has long
been recognized as a disturbing feature of this disease. Not only do the
symptoms of celiac disease wax and wane but also the damage to the intestinal wall seems to vary.
This has several important implications. It suggests that we should
treat any person with positive blood tests, but negative biopsies, as potential celiacs. More specifically, it questions whether or not these "false
positive" anti-gliadin blood tests are meaningful or helpful. It also reveals
a problem with intestinal biopsies as a diagnostic tool. As long as we accept the notion that such biopsies provide a gold standard for diagnosis,
it should alert us to the need for regular and repeated testing.
NON-CELIAC GLUTEN SENSITIVITY
A similarly broad range can be found in non-celiac gluten sensitivity. Simply put, those people who have a nonspecific injury to the intestinal mucosa that leaks food proteins and toxins into the blood but do not have
the damaged villi and/or increased intestinal immune cells found in untreated celiac disease can be said to have non-celiac gluten sensitivity.
Identification of this form of gluten sensitivity is as simple as getting a
blood test for specific antibodies. Non-celiac gluten sensitivity afflicts about
20 percent of the American and Canadian population and, along with the
telling elevated antibodies against gluten, can be found in most of the
same ailments that are overrepresented among untreated celiacs.
DERMATITIS HERPETIFORMIS—AN
EXAMPLE OF BOTH CELIAC AND
NON-CELIAC GLUTEN SENSITIVITY
Dermatitis herpetiformis is a lifelong gluten-sensitive skin disease. Also
known as Duhring's disease, this fascinating subgroup of celiac disease
42
Dangerous Grains
Thirty-Three Years of Itching
Ends with a Gluten-Free Diet
developed an itchy rash starting on my elbows my senior year in
college. Over several months the rash spread to my knees and
different parts of the rest of my body. This was in the mid-1960s.
I visited many doctors, an allergist, and several dermatologists over
the years.
Over thirty-three years after the rash started, I happened to see
an article in Prevention magazine describing the case of a woman
with dermatitis herpetiformis. I had never heard of celiac disease,
dermatitis herpetiformis, or gluten before. I got on the Internet,
and within fifteen minutes I knew that I had this gluten-induced
skin disease. It was a classic case. I immediately went on a glutenfree diet, and on the third day, I stopped itching for the first time in
over thirty years.
I then saw a gastroenterologist. I looked too healthy to be a
celiac. He agreed to do a blood test, and after a little research he
agreed to do a biopsy. Both the biopsy and blood test were positive
for celiac disease. It took a few months for the rash to totally clear
up. I also had a number of digestive and gynecological problems
go away.
Barb W.
shows itself primarily on the skin. The most common locations for these
lesions are the back of the knees, buttocks, elbows, and the face.
Sometimes in the form of a rash and sometimes in the form of multiple pimplelike lesions, dermatitis herpetiformis is usually extremely itchy.
The rash or lesion is usually symmetrical—that is, if there are one or two
itchy lesions on one buttock or leg, there will soon be the same number
Types of Celiac Disease and Non-Celiac Gluten Sensitivity
43
in the same approximate location on the other side of the face. Dermatitis herpetiformis lesions often develop following exposure to sunlight or
iodine. A primitive and unreliable means of diagnosing this condition is to
soak a patch of fabric in iodine and tape it to the skin. If a lesion developed, dermatitis herpetiformis was diagnosed. Today's diagnostic procedures are much more accurate.
About 75 percent of individuals with this gluten-induced skin condition show intestinal damage on biopsy. It is important to recognize that
the increased risks of cancer and other sequelae of dermatitis herpetiformis are about the same as those associated with untreated celiac disease. Many researchers consider dermatitis herpetiformis to be a skin
manifestation of celiac disease and maintain that improved testing techniques will reveal gluten-induced intestinal damage in all cases of this
skin disease.
There is little to be gained, other than convenience, by continuing to eat
gluten in the context of dermatitis herpetiformis. Yet, few dermatologists
recognize this disease, and all too often those who do continue to recommend drag treatment in place of dietary intervention, oblivious to the
danger of cancer, which is only preventable with a gluten-free diet. Such
drug treatment may control the symptoms of this disease; however, the
insidious, gluten-induced damage to tissues, organs, and body systems will
continue.
RANGES OF SENSITIVITY
IN CELIAC DISEASE
An important consideration, especially when developing an understanding of celiac disease, is to recognize that, while the health risks appear to
remain constant for people with celiac disease, the symptoms do not.
This means that some people with celiac disease will be exquisitely sensitive to the slightest quantity of gluten, while others may eat significant
quantities of gluten with little or no apparent response.
On the surface, this might suggest that some celiacs can eat gluten
44
Dangerous Grains
safely. But the research does not support that perspective. This is an area
where we still have a great deal to learn, but it appears that there is variability in how much of the intestine is affected by gluten. According to
one report, less than one gram of gluten daily is sufficient to perpetuate
intestinal damage in a celiac. The range and variability of symptoms also
suggest that there are many individual differences from one patient to
the next, particularly regarding the region of the small intestine that is affected by gluten.
An Extreme Reaction to Gluten
I
n 1991 1 started having digestive symptoms and losing weight.
My doctor started testing. Eventually, during a visit to the doc-
tor, 1 mentioned that I seemed to feel better in the morning if I
ate Cream of Rice cereal. The doctor mentioned that there was a
rare disorder called celiac sprue and urged me to try a gluten-free
diet. I did start feeling better for a while—but not for long. The
weight loss continued. I started becoming "clumsy." I'd drop things
and seemed to trip over my own feet. My hands and feet began to
feel like they were rubber rather than skin. 1 lost more weight.
With more meds and continued testing, 1 had so much abdominal
pain that it was difficult to function, I was exhausted all the time,
and I started having panic attacks. I lost 85 of 215 pounds. I am
a tall woman—but I looked like a concentration camp survivor.
I also experienced spontaneous bruising. I could watch as a spot on
my arm or leg would swell, hurt like heck, and then turn vibrant
purple.
In January 1992 I was hospitalized. 1 could barely use my left
hand, I was cold all the time. It was all I could do to stay awake. I
was having severe head pains and still losing weight after more
Types of Celiac Disease and Non-Celiac Gluten Sensitivity
45
testing. A psychiatrist was called in. He announced I had what was
then called a major affective disorder (depression). I was counseled for anorexia. My guts hurt, my bowel movements were foul,
and I was tired of trying to stay alive.
Though still on a gluten-free diet, I was worse than when the
doctor first suggested celiac disease. My salvation came when a
hospital dietitian was monitoring my food intake due to suspicions of anorexia. The dietitian brought me a photocopy of a
booklet about celiac disease. On the last page there was a blurb
about making sure your medications had been checked to assure
they did not contain gluten. A call to the pharmacist confirmed
that nine of the eleven medications I was taking contained gluten.
As soon as I stopped taking all but my thyroid medications, I
started getting better.
Slowly I got my energy back. I started feeling human again. My
body had deteriorated so much that it had been devouring itself
in an attempt to find protein. I was starving to death, and if this
had continued much longer, my body would have not been able to
restore itself. I was lucky.
DeniW.
APPLICATION OF CELIAC RESEARCH
TO GLUTEN SENSITIVITY
Only a little research has been conducted in the broader realm of gluten
sensitivity. We therefore rely heavily on the research into celiac disease to
deduce risks and prognoses. Researchers working in this area commonly
test for, and report, levels of anti-gliadin antibodies among their subjects.
We have therefore generalized findings from celiac disease to the larger
population of gluten-sensitive people. There are several problems with
our approach. It is impossible to say that all individuals who are gluten
46
Dangerous Grains
sensitive will suffer the same risk of a given disease as those with celiac
disease. This possibility of a reduced risk raises some important questions. Just how strictly should we exclude gluten from the diet? What are
the economic and social implications of gluten exclusion? Despite these
questions, some of the best-informed scientists investigating celiac disease have arrived at a position similar to the one we are taking. They argue for a shift away from the current focus on celiac disease, to explore
gluten sensitivity more fully.
The world-renowned researcher Michael N, Marsh has argued for redefining celiac disease and changing the name to "gluten sensitivity." He
has also pressed for defining this disease exclusively on the basis of immune reactions to gluten. Dr. Marsh limits his discussion of the immune
responses to gluten that can be identified from changes in the intestinal
wall following direct contact with gluten.
On the other hand, others have:clearly shown that many types of human tissues are damaged when they come in contact with gluten. If we
are mounting an immune response to gluten, it is reasonable to conclude
that we are leaking some of these proteins or derivative peptides into our
blood. If they are reaching the bloodstream, then a wide range of tissue
damage is predictable.
Rather than ignoring chronically ill, non-celiac gluten-sensitive individuals who show no tissue damage on biopsy, we suspect that any and
all identifiable immune responses to gluten should be recognized as dangerous. The evidence strongly suggests that everyone mounting such an
immune response should be encouraged to strictly exclude all gluten
from his or her diet.
3
Proactively Determining
Your Risk
G
luten grains are a leading cause of many ailments. Avoiding gluten
prevents and often reverses these diseases. Should you passively wait
for the signs and symptoms of disease to arrive before taking action?
There are many cases of apparently healthy individuals who seem to suddenly succumb to celiac-associated cancers, autoimmune diseases, or other
serious celiac-associated ailments, although there is little prior indication
of the underlying disease.
Fortunately, there are rational alternatives. With the help of simple,
affordable blood tests that are available to all health consumers, you
can now determine your genetic makeup and the presence or absence of
antibodies indicating gluten sensitization and celiac disease. In addition,
armed with the information in this book, you can examine your own
family and medical history for evidence of a gluten problem.
None of these sources can conclusively diagnose celiac disease or
gluten sensitivity. However, the patterns formed by an orderly examina-
48
Dangerous Grains
Hon of information drawn from all of these areas will reveal your own
unique risk of developing one or more gluten-induced ailments.
Information on relevant testing and when to eliminate gluten from
one's diet will follow in later chapters. Understanding what signs indicate
risk and how to evaluate your own unique pattern of risk is the most
important first step toward preventing, arresting, and/or reversing gluteninduced illness. The cause of many symptoms and complaints often becomes obvious in hindsight, yet it remains obscure to those of us who still
consider wheat to be the staff of life.
SELF-EXAMINATION
In your search for clues and warning signs, thefirst place to look is within.
You know your own moods better than anyone. You know your cravings
or addictions. You know your own habits. You are probably more aware
of your appearance and stature, too. Who could know your sleep requirements and energy levels better than you? And what about your perceptions, minor pains, abdominal bloating, and your susceptibility to colds or
the flu? Each of us is our own best expert when it comes to ourselves.
Questions to Ask Yourself Now, Rather than Later
1. Is there anyone in your immediate family who is a proven celiac or
is gluten sensitive?
G yes G no
If yresr you are at high risk of having or developing gluten problems,
2. Are you or is any member of your immediate family a victim of
an autoimmune disease such as insulin-dependent diabetes, autoimmune thyroid disease, or Addison's (adrenal) disease?
Q yes G no
Proactively Determining Your Risk
49
All of these conditions are commonly found in celiacs and their
family members.
3. What are your eating habits? Do you have food cravings?
•
yes
O no
If so, what foods do you crave?
If dairy products or foods with high levels of gluten are on your
list, we suggest that you seek testing for celiac disease and food allergies. Because some of the partial proteins from gluten and dairy
products can be highly addictive, if they are regularly absorbed into
the circulation, cravings for these foods are cause for concern.
4. After meals, do you often feel bloated and uncomfortable? Do you
have to loosen your belt? Is breathing more difficult? Is the bloating often associated with an inexplicable gain of two to five pounds
within a twenty-four-hour period?
•
yes
• no
5. Have you ever had one or more bouts of severe abdominal
cramping?
•
yes
• no
If you have celiac disease or gluten sensitivity, such cramping can
sometimes be so severe that it leads to shock. In such cases there is
always a gluten-induced potassium deficiency, often accompanied
by magnesium and/or calcium deficiency.
6. Do you have strange or addictive reactions to alcohol?
•
yes
• no
Either may also signal gluten sensitivity. We know that alcohol
causes and aggravates a leaky gut; many authorities believe that a
50
Dangerous Grains
leaky gut is a common cause as well as a consequence of food allergies and gluten sensitivity.
7. Are you a smoker?
• yes • no
A powerful tobacco addiction can also signal gluten sensitivity.
Smoking can amount to a lorm of neurochemical "self-medication"
for those who have problems with gluten. Smoking delays diagnosis and allows the progression of the disease. Such addictions
are very difficult to break because quitting means more than simply dealing with the Meeting experience of withdrawal. It will
bring about a reduction in general health and, in many former
smokers, major depression—which will persist until the underlying problem with gluten is diagnosed and treated.
8. Do you struggle with anxiety and/or depression?
•
yes U no
These are common signs of gluten sensitivity.
9. What about your visual perceptions? Have you ever been sitting
quietly, staring into the distance when things appeared much more
distant than is possible? Or maybe they were distorted?
•
yes Li no
If you have had such sensations, you may well have a problem
with gluten.
10. What about your sleep habits? Do you usually have difficulty getting to sleep?
• yes
• no
Proactively Determining Your Risk
51
11. Do you have an excessive need for sleep?
G yes
Q no
12. Are you disoriented and confused when you awaken?
•
yes • no
13. Do you have to get up frequently during the night to urinate?
G yes Li no
14. Are you, or have you ever been, a bed wetter?
Q yes Q no
Such patterns suggest a problem with gluten, dairy proteins, or
both.
15. Do you often have difficulty finding the energy for life's daily
demands?
•
yes • no
Your body may be giving you an early warning. Lethargy of unknown cause is another common sign.
SHORT STATURE IS YET ANOTHER
IMPORTANT SIGN OF A PROBLEM
W I T H GLUTEN
Several physical features, including your height and weight, can identify
significant risk factors. People of below normal height, and especially children in the lowest 10th percentile, should, in the absence of a solid medical explanation for their stature, consider testing. Because susceptibility
Dangerous Grains
to the hazards of gluten is largely genetic, even where short stature appears to be a family trait, the possibility that gluten is an underlying cause
in all family members should not be ignored.
Short stature and growth retardation can provide important warnings.
Just as reduced stature was part of our ancestors' transition to agriculture,
growth stunting continues to be a factor in celiac disease. In fact, half of
all young celiacs over the age of two years are short compared to their
peers.
There are many reports of short stature in connection with undiagnosed celiac disease. Some groups report rates of undiagnosed celiac disease in about one quarter of the subjects studied. Others report that as
many as half of the individuals of short stature, when the cause of their
short stature was unknown, have been diagnosed with celiac disease
when tested. Little wonder that these researchers repeatedly urge testing
all people of short stature for celiac disease. Even where growth hormone
abnormalities are found, celiac testing is warranted because gluten can
suppress growth hormone release.
OBESE CELIACS NO LONGER
A CONTRADICTION
Obesity is another warning sign that gluten may be at the root of your
difficulties. Despite the long-standing perception that celiac disease leads
to frail, wasting, undernourished individuals, there are more obese and
overweight celiacs than underweight. This is revealed through random
testing for celiac disease.
MAKING USE OF REGULAR
MEDICAL CHECKUPS
There are also a number of important warning signs that commonly
show up in the routine lab tests done at the time of your annual medical
Proactively Determining Your Risk
checkup. These test results, when low-normal levels or deficiencies are indicated, will alert and benefit those with a high index of suspicion of
celiac disease and gluten sensitivity.
Even when blood values approach the boundary of the normal range,
those that should be carefully checked include:
• iron deficiency and iron deficiency anemia
• folate deficiency
• elevated free homocysteine
• vitamin B, 2 deficiency
• elevated or high-normal serum alkaline phosphatase often associated
with gluten-caused bone loss (interestingly, zinc deficiency, often
found in celiac disease, is commonly associated with low-normal alkaline phosphatase)
• chronically elevated liver enzymes of unknown cause
• low or low-normal serum albumin
If you suffer from chronic iron deficiency or iron deficiency anemia, or
if regular iron supplementation just keeps your results at the low end of
the normal range, there is cause for concern. The part of the small intestine where most iron is absorbed is the same part of the intestine where,
in celiac disease, the greatest damage is often caused by gluten. Hence,
iron deficiency anemia of unknown cause should routinely lead to testing
for problems with gluten.
Folate is a B vitamin that is critical to neurological development and
maintenance and is often depleted among those with untreated celiac
disease. In order to prevent spina bifida, folic acid supplementation is of
prime importance to women wishing to become pregnant. Low folate
levels should alert us and should encourage appropriate testing.
An excellent predictor of risk for heart attacks and strokes is the level
of free homocysteine in your blood. It may be elevated in as many as
30 percent of all people with a history of heart attacks. As with cholesterol and blood-pressure measurements, routine testing for homocysteine
should be part of your annual physical. When it is high-normal or elevated,
54
Dangerous Grains
this is cause for concern. The good news is that these levels indicate deficiencies of folate, vitamin BG, and/or vitamin B | Z , which can often be
remedied by supplementing a high-potency B complex. It may also be an
indication of underlying celiac disease, known to cause such deficiencies.
When one's homocysteine does not respond well to B vitamin supplementation, gluten sensitivity should be considered as a cause. For people
with such deficiencies, a strict gluten-free diet might be just what the
doctor ordered.
YOUR MEDICAL HISTORY
In addition to monitoring your routine test results, examination of your
medical history can also be very revealing.
Low Blood Pressure
Chronically low blood pressure, defined as a systolic pressure of under
90 and a diastolic of less than 60, is also common among celiacs and
should signal concern if your medical records reveal such a history. All too
often, this is touted as a sign of good health when it actually may indicate
a serious problem with gluten. Low blood pressure is usually accompanied by an inclination to fainting and sensations of light-headedness. A
significant minority of celiacs will also demonstrate elevated blood pressure, so absence of low blood pressure should not be taken as a means of
ruling out celiac disease.
Heartburn, Esophageal Reflux
If your history reveals that you have repeatedly been given medications for heartburn, or today what is fashionably called esophageal reflux,
there may be cause to suspect celiac diesease. Similarly, if you are one of
the many Americans who frequently consume over-the-counter antacids,
testing for celiac disease may be very helpful.
Proactively Determining Your Risk
55
Vitamins C and K, Bleeding and Bruising
Some researchers believe that the condition of vitamin C deficiency—
scurvy—is common among children with celiac disease and can result in
bleeding in the bowel or under the skin, or both. Vitamin K deficiency
can also cause a wide variety of bleeding problems and may be the cause
of some of the cases of intestinal hemorrhaging or bleeding following dental surgery that have been reported in people with celiac disease. Patches
of red or purple rash are found in about 10 percent of newly diagnosed
celiacs and may be the result of either of the above deficiencies or an
autoimmune disease where there is a deficiency of blood platelets.
Looking for Mineral Deficiencies
Despite ample intake of dietary minerals, some people with undetected gluten sensitivity suffer from multiple deficiencies. Because of the
inflammatory erosion of the intestinal lining, they are not absorbing these
minerals well. Their bones become weaker, they grow very slowly, they
perform poorly in school, they are more likely to become anemic, they
heal more slowly, they begin to complain of chronic pain syndromes, and/
or their immune systems fail to protect them from recurring infections.
One common denominator with all of these conditions may be a lack of
adequate iron, zinc, magnesium, selenium, and/or calcium for proper immune function. In the absence of trauma or dangerous infection, these
people may often appear healthy.
Coughing, Wheezing, Shortness of Breath,
and Gluten
A wide range of lung problems, including chronic bronchitis and asthma,
characterized by chronic wheezing, coughing, shortness of breath, or difficulty in breathing, are commonly caused or made worse by gluten. Researchers are reporting that one-third of celiac patients have respiratory
allergies. From a variety of allergic lung conditions, to defects in the lining
Dangerous Grains
of airways, to ulcers on the lung walls, to diffuse bleeding in the lungs and
chronic obstructive pulmonary disease, gluten-related problems abound
in asthma. Poor breathing from lack of adequate oxygen exchange is often the result. Lung disorders found in association with celiac disease
sometimes show, on biopsy, evidence of a mucosal defect in the lungs that
is similar in appearance to that found in the intestines. Therefore, chronic
lung disease should also signal concerns about an underlying problem
with gluten. We recommend that anyone with respiratory allergies get
tested for gluten sensitivity.
Other Signs from Your Medical History
If you have struggled with repeated bouts of multiple, very painful
sores inside your mouth, called aphthous ulcers or canker sores; if your
fifth fingers are short and palms orange; if your fingertips are clubbed; if
your fingernails are thin, brittle, and spoon-shaped; or if your nail beds
remain pale when compressed, any of these can signal the presence of
celiac disease or gluten sensitivity.
ARE YOU A MEMBER OF A
HIGH-RISK GROUP?
Your medical history will also include specific ailments and diseases. Such
conditions can warn of gluten sensitivity even when they appear to be
unrelated. There are several general categories of illness where gluten
sensitivity should be considered. They are:
• allergies
• autoimmunity
• bowel disease
• cancer
• growth retardation
• learning disorders
Proactively Determining Your Risk
57
• lung disease
• psychiatric ailments
• reproductive problems
• seizures
High-Risk Candidates for Celiac Disease—
Are You One of Them?
d ]
1. All first-degree family members of those with non-celiac gluten
sensitivity or celiac disease. Some now argue for testing seconddegree relatives.
2. All insulin-dependent diabetic (IDDM) patients and all firstdegree relatives of these patients.
3. All autoimmune thyroid patients (both underactive and overactive) and all first-degree relatives.
4. All patients with chronic neurological or neuromuscular conditions of unknown cause (e.g., ataxia and peripheral neuropathies).
5. All patients with chronic liver disease/abnormally elevated liver
enzymes of unknown cause. This includes primary biliary sclerosis, the disease that recently resulted in the premature death
of NFL football legend Walter Payton.
6. All osteoporotic children (e.g., children suffering from frequent
or easy/low impact bone fractures).
7. All postmenopausal osteoporotic women unresponsive to conventional therapies.
8. All epileptics with histories of migraines, ADHD, and/or calcium deposits in brain tissue.
9. All individuals suffering from chronic severe headaches unresponsive to conventional medical intervention, especially those
with associated complaints of dizziness or imbalance.
continued
58
Dangerous Grains
10. All patients with iron deficiency or iron deficiency anemia of
unknown cause.
11. All pregnant women, especially those with a history of infertility, miscarriage, low birth weights, anemia, or other unfavorable pregnancy outcomes.
12. All children being considered for a diagnosis of ADHD.
13. All children with learning disorders.
14. All CD patients supposedly on a strict gluten-free diet, but
with persistent or recurring symptoms.
15. All patients with Down syndrome,
16. All people with Turner's syndrome.
17. All people with major depression unresponsive to conventional
antidepressantmedication.
Your Work History
Your line of work, past and present, can also be an important factor in
determining your risk of gluten sensitivity. Among flour mill and bakery
workers, researchers have found dramatic increases in IgG class antibodies
against gluten, the same antibodies that form from eating gluten. Their
findings suggest that people working with flour are more likely to develop a systemic immune response to gluten through a reaction in the
mucus that lines the lungs.
Your Family Tree
When examining your family health history, the presence of any of
the ailments that are found more commonly in celiac or gluten-sensitive
patients should also alert you to the possibility of your own increased risk
of celiac.
Dr. Chris Reading and Ross Meillon of Australia have provided an ex-
Proactively Determining Your Risk
59
Family History of Celiac Disease,
Eight Years of Chronic Diarrhea, and
Finally a Diagnosis ...
he day I received my celiac diagnosis, I cried. After eight
years of steadily increasing diarrhea, I finally had the answer.
I had been through so many tests. I initially blamed my ailments
on drinking some bad water when visiting my sister in Texas shortly
after my second child was born in 1991 I had mentioned several
times to my family doctor that my father had celiac disease, but
it wasn't until November 1999 that I asked to be tested for celiac.
I was diagnosed after an endoscopy and biopsy.
I also cried that day because 1 was sad. My father got so sick he
died at age sixty-six from complications of celiac disease. He didn't
have the resources we have today. He was handed a small book of
recipes from the Hospital for Sick Children, Toronto, Canada. He
researched in the library, I am sure, but he missed out on the wonderful connections of the Internet.
I often wonder if the lack of nutrients in my body caused me
to contract breast cancer at age thirty-seven. All of my doctors
said there was no connection, but I saw my father go through
chemotherapy when he ended up having lymphoma. I often wonder if they are just not sure. My tears flow so easily anymore. E was
feeling so abnormal and so sick—I can understand fully why people
turn to antidepressants with this condition. I have found the silver
lining to this black cloud and am living a fuller life now.
Lynn P.
60
Dangerous Grains
cellent guide for developing an informative chart of your family's health
history in their book Your Family Tree Connection. There is plenty of evidence to support such an approach. Almost half of the close relatives of
celiac patients have increased intestinal permeability and, hence, a greater
likelihood of both gluten sensitivity and celiac disease. Cancer also strikes
family members of the celiac patient more often than others.
By beginning to think about disease susceptibility in light of one's
family and, hence, genetic background, a wide range of preventive strategies becomes an active part of one's life. For instance, if a woman has given
birth to a child with spina bifida, there is a clear case of folate deficiency
and, hence, an increased risk of celiac disease in the mother. Further, one
out of every fourteen patients with Down syndrome has undetected celiac
disease. If you have a child with Down syndrome or a child with spina
bifida, testing for gluten sensitivity and celiac disease is the next logical
step.
If you are a member of one of the groups of people who have an unusually high risk of having or developing celiac disease, you absolutely should
be routinely tested for both gluten sensitivity and celiac disease. Due to
concern about latent celiac disease, if the initial blood screening is negative, you should schedule to be tested again every few years.
The patterns of information drawn from these five areas of your life
and your family history offer a clear sense of whether you should seek
testing for gluten sensitivity and celiac disease. The next chapter offers information about the wide variety and relative value of these tests.
Testing for Gluten Sensitivity
in All Its Forms
N
ow that you have a sense of what your risk might be, you will want
to choose a test or series of tests appropriate to your risk, concerns,
and budget. This is an issue that appears simple enough, but it is a little
more complicated than that. There are several important mistaken beliefs
about celiac disease that should be corrected. For instance, we have heard
from individuals who were being investigated for celiac disease, but they
were already on a gluten-free diet. With one important exception—a rectal challenge—there is no diagnostic procedure yet known that will reliably identify celiac disease after the patient has been following a strict
gluten-free diet for just a few weeks. Sometimes testing is unreliable after only a few days. This chapter offers information that explains the various tests that can address your unique needs, and it will guide you past
the many pitfalls of testing.
62
Dangerous Grains
WHAT ARE YOU LOOKING FOR?
There are a variety of tests that will identify gluten sensitivity or celiac
disease. Some tests will identify one condition while suggesting the other,
while other tests will only identify or suggest one form of gluten problem. From a wide range of blood tests; to skin, rectal, and intestinal biopsies; to genetic testing; to saliva testing, our responses to gluten can be
tracked in a number of ways. Each form of testing has its own unique
strengths and weaknesses. Each offers important insights into how we react to gluten, so your choices should be shaped by your individual needs
and test availability.
Issues of cost, convenience, and comfort may also be important in
making the right selection. Because we are all unique and each of us reacts in a slightly different manner, it is not satisfactory to rely on a single
form of testing. Your choice should be based on your unique needs and
circumstances, not your doctor's convenience or level of knowledge. For
instance, people whose siblings have been diagnosed with celiac disease
might choose testing to determine if they have the genetic HLA markers
for celiac disease or gluten sensitivity. A negative test will tell them all
they need to know—that they have little risk of ever developing a problem with gluten. A positive test, on the other hand, will often indicate
that this particular family member either has, or may soon have, an identifiable problem with gluten.
IMPORTANT ANSWERS TO BE FOUND
IN HLA-DQ GENETIC MARKERS
Since genetic testing of your white blood cells is becoming increasingly
available, you and your family may wish to make use of this important
blood test to determine your inherited propensity to develop gluten sensitivity and/or celiac disease.
Testing for Gluten Sensitivity in All Its Forms
63
Dr. Kenneth Fine, a world-class researcher in this area, recently stated
that HLA-DQ2 and/or HLA-DQ8 is present in about 43 percent of the
normal American population. Dr. Fine believes that if one has such a genetic predisposition for developing a gluten-induced disease, the wisest
approach is to avoid this disease-causing food.
In some cases, however, genetic testing may have little value. Those
with non-autoimmune thyroid disease, for instance, have about the same
risk of showing these genetic markers as any member of the general population. Such a person would benefit more from examining their risk factors, as outlined in the previous chapter, to determine whether there is
any need to be concerned about gluten. If there is cause for concern, a
more specific test should be chosen.
SMALL INTESTINAL BIOPSY
One individual contacted us reporting that she had been reassured that it
takes four to six months for gluten-induced intestinal damage to heal, so
a biopsy will identify celiac disease for up to six months after beginning a
gluten-free diet. While it is true that it can take that long or longer for
gluten-induced injuries to completely heal, it is a mistake to believe that
a biopsy can produce an accurate diagnosis when consuming a glutenfree diet.
The biopsy is simply a sample of the cells in the intestinal wall. These
cells are completely replaced every few days. This rapid replacement
lends itself to extremely rapid healing of the very region that is being
examined for injuries that are signs of celiac disease. In many cases, the
intestine will appear perfectly normal after just a week or two of strict
compliance with a gluten-free diet.
Everyone with a healthy intestine has millions of fingerlike projections on their intestinal wall called "villi." They improve the absorptive efficiency of the intestine by increasing the surface area through which
nutrients can be absorbed. The flattening of all villi would reduce this
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Dangerous Grains
surface area to a fraction of that of a healthy intestine. Such a reduction
of surface area will cause a substantial failure to absorb nutrients from
the food that passes through the intestine.
The current test that is touted as the "gold standard" for the diagnosis
of celiac disease is a biopsy, taken by endoscopy. It is a process where a
tube is passed down the throat, through the stomach, and into the small
intestine. Tiny tissue samples are then taken from the intestinal wall for
examination under a microscope, if the biopsy shows a flat surface, and a
gluten-free diet shows in improvement on a second biopsy, then celiac
disease is diagnosed.
This procedure was once without much controversy. When only those
with a flat intestinal wall were considered candidates for a diagnosis of
celiac disease, this disease was thought to be rare.
But this is not accurate because of the range of damage that can signal
celiac disease. Dr. Michael N. Marsh has devised an ingenious system for
categorizing the stages of gluten-induced damage to the intestinal wall.
It not only offers a standardized approach to evaluating intestinal biopsies for the diagnosis of celiac disease but also encourages a fuller understanding of the immune mechanisms at work in celiac disease.
The Marsh system aids diagnosis of immune reactions to gluten that
result in a range of damage to the intestinal wall. Because celiac disease is
so variable, a more dynamic system for reading biopsies was necessary.
Celiac symptoms wax and wane, and damage to the intestinal wall varies
from one location to the next, and with the passage of time. The Marsh
system has captured the range of intestinal damage that can result from
celiac disease in a simple way that allows pathologists to uniformly identify the presence or absence of this disease. With the exception of Type 0,
which depicts healthy tissue, from Type 1, indicating an infiltration of immune cells called intraepithelial lymphocytes, to Type 4, indicating tissue
damage that is very resistant to treatment, each category of tissue damage
indicates a level of intestinal injury that is commonly found in celiac disease. Celiac disease may thus be identified at an earlier stage and from
biopsies that would previously have been viewed as inconclusive.
Testing for Gluten Sensitivity in All Its Forms
65
If you envision the inside of the intestine as the area above each of the
biopsy samples depicted above, you can see that less surface area is available for nutrient absorption, as the gluten-induced damage progresses.
Type 3 and 4 lesions are quite flat.
There is currently considerable variation in perspectives, from one pathologist to the next, regarding the signs that suggest the possibility of
celiac disease. Some pathologists have insisted that their job is simply to
describe the microscopic appearance of these tissues without ever suggesting the possibility of celiac disease. The Marsh system removes this
problem by providing a set of templates for evaluating biopsies and providing clear guidelines and criteria for when to consider celiac disease.
In the past, the gastroenterologist or endoscopist often relied on the
pathologist to raise the question of celiac disease, and the pathologist
awaited the suggestion of celiac disease from the gastroenterologist. Despite clear signs, it was often never mentioned. Little wonder celiac disease
was so rarely diagnosed! Thanks to the Marsh system and other advances
in diagnostic testing, the number of such errors should diminish.
GLUTEN CHALLENGE
A gluten challenge is the process of consuming multiple daily servings of
gluten-rich foods—as is common in the average Western diet—in order to
gauge the body's reaction. Breakfast, for example, would likely include
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toast or cereal. Snacks might be cookies, crackers, muffins, or pastries.
Lunch might contain sandwich bread or pizza, and the evening meal might
include pasta, piecrust, or Yorkshire pudding, along with a flour-thickened
gravy.
The major pitfall of such a gluten challenge is that it is often undertaken by those who have been following a gluten-free diet as the result
of their own research or on the advice of a health-care practitioner or
friend. Whether motivated by the difficulty of the gluten-free diet, concerns for family members, issues related to insurance coverage, income
tax considerations, or other factors, such individuals later want laboratory
or biopsy confirmation from a doctor for the diagnosis of celiac disease.
But, if a patient has already begun a gluten-free diet and the intestinal
wrall has thus been given a chance to heal, it can take as much asfive years
or more after returning to eating gluten before the intestinal damage characteristic of celiac disease will show up on a biopsy. It is often too late to
obtain a biopsy-based diagnosis except through a rectal challenge, which
is discussed later.
SUGAR-ABSORPTION TEST
FOR LEAKY GUT
The sugar-absorption test does not diagnose any disease. It is often used
to identify increased intestinal permeability, or "leaky gut." The test is
based on recognition of the complex interactions between several indigestible sugars called "disaccharides" and the function of different parts
of the gastrointestinal tract. We are unable to metabolize these sugars,
so whatever we absorb into our blood will be excreted in our urine. In
a healthy person, after swallowing measured amounts of the sugars—
lactulose and mannitol—insignificant quantities of them should be absorbed into the bloodstream.
Because molecules of each of these sugars have different properties,
even wrhere there is inappropriate intestinal leakage, more of one sugar
Testing for Gluten Sensitivity in All Its Forms
67
will be absorbed and pass into the urine unchanged, thus identifying the
leaky gut, along with the location of its greatest permeability.
Even the most vocal advocates of this test are unlikely to see it as a definitive test when used in isolation. However, it is a valuable adjunct to
other testing. For instance, this test can make a second intestinal biopsy
unnecessary for confirming a celiac diagnosis. Reduced intestinal leakage,
after about a month on a gluten-free diet, will confirm the diagnosis. It is
also a valuable companion to screening blood tests, providing a clearer
picture of the condition of the intestine.
The sugar-absorption test is limited to identifying relative improvements. The improved state in one patient may still exceed the degree
of leakiness found in an untreated celiac patient. It is also limited by another factor. Alcohol consumption, antibiotics, steroids, nonsteroidal antiinflammatory drugs, many non-gluten food allergens, spices, hormonal
variations, infections, injuries, surgeries, and many conventional cancer therapies can alter intestinal permeability very rapidly. The sugar-absorption
test is designed to identify only a current state of increased intestinal permeability. Results of this testing can therefore be quite misleading, as
there are so many other factors in addition to celiac disease that are not
controlled in the context of this testing that can exert a substantial influence on the test results.
BLOOD TESTING
The reliance on intestinal biopsies may soon be a thing of the past. Extremely specific and reproducible blood testing is poised to take its place.
Some of these blood tests offer the added advantage of identifying people
who are mounting an immune response, regardless of intestinal damage.
Other tests will only identify advanced celiac disease. There is quite a range
of tests, offering considerable choice to health-care consumers. The development of blood tests that can identify the antibodies relevant to gluten
sensitivity may well be one of the greatest scientific leaps of the last century.
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Anti-Gliadin Antibody (AGA) Blood Test
If you put gluten in a petri dish with human internal organs, the
gluten damages these tissues. If a gluten-sensitive individual consumes
gluten, he or she runs the risk of damaging organs and tissues throughout
the body. Therefore, finding out if gluten is getting into your bloodstream
and creating havoc makes good sense. Now, recall that gliadin is an important but very troublesome member of the family of gluten proteins.
Testing for antibodies produced and directed against gliadin is currently
one of the best ways to determine whether gluten is getting into our
blood and, hence, if we are in danger.
Our immune systems can't tell the difference between a gluten protein and another foreign protein that is a structural part of bacteria or a
virus, so we react the same way against all foreign proteins, by developing
specific antibodies against these proteins. Two classes of antibodies that
are sensitized to gliadin are sought in antibody testing. These classes are
identified as IgG and IgA antibodies.
Importance of Testing for IgG and IgA
Anti-Gliadin Antibodies and IgG Antibody
The most common criticism of AGA blood tests is that they are not
specific enough. Elevated levels of gliadin antibodies are found in many
people with a variety of ailments, many of which do not include celiac disease. They are even found in apparently healthy people. Because of this,
such abnormal AGA results are often dismissed as meaningless. The IgG
class of antibodies is by far the largest group of antibodies in the human
body. These antibodies don't identify any specific disease and are often
found elevated in people who have few or no symptoms. And they do last
a long time, especially compared with other classes of selective antibodies. A comparatively brief period when there is leakage of gluten into
the bloodstream could result in a positive AGA blood test for up to six
months or so.
How, you may ask, is this test useful? It identifies a leaky gut. Unlike
Testing for Gluten Sensitivity in All Its Forms
69
the sugar-absorption test, it identifies any relatively recent event of significantly increased intestinal permeability when gluten proteins were
leaked into the bloodstream.
IgG is a test that also warns of the likelihood of additional delayed-onset
food allergies and the possibility of toxic-liver overload. It may also point
Gluten Sensitive and Food Allergic—
Diagnosed with Blood Tests
I
developed a concave area on my back at about the level of my
kidney. It was slowly growing in size and had become veiy painful.
Our family doctor suggested that it was some kind of fatty tissue
necrosis. I visited three different specialists. Each of them admitted
that they were unable to offer a treatment that would reverse or
halt the disease. They could not even identify it. I was given pain
medications. I slept through the night, and much of the day. I
gained weight from my inactivity. I was depressed and barely able
to look after my two children, who were six and eight years old at
the time.
Because the doctors were stumped, I had blood drawn and sent
off for testing for celiac disease. I had elevated gliadin antibodies.
Our doctor was skeptical about the value of these tests.
I then had blood drawn for IgG ELISA testing, which revealed
sensitivity to gluten, dairy, and seventeen other foods. Within a
week of eliminating the identified offending foods, the pain disappeared. I discontinued the pain medications and needed less sleep.
The following week, the concavity became itchy. The afflicted area
began to shrink.
Even now, if I accidentally eat gluten or dairy, I develop
joint pains.
Kari K.
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Dangerous Grains
to the source, or a contributing factor, in a current disease state. More important, it signifies that an individual has become sensitized to gliadin and
is at risk of gluten sensitivity or any of the forms of celiac disease.
All patients with elevated IgG and/or IgA antigliadin antibodies should
be treated seriously and monitored carefully. All such individuals should be
routinely blood tested for celiac disease.
IgA Antibody
Another class of gliadin antibody that is easily identified, and often
quite useful, is the IgA antibody. It is usually much shorter lived than the
IgG antibody. This makes it very useful for monitoring dietary compliance. However, it is also valuable, especially in combination with IgG
antibody testing, for screening large groups when looking for celiac disease. These anti-gliadin antibody blood tests are comparatively inexpensive, and when used together they are quite good at identifying those who
should be biopsied and tested for endomysium antibodies.
Endomysium Antibody (EMA) Testing
Endomysium is connective tissue that sheaths certain muscle fibers.
The development of the endomysium antibody test resulted from recognition that antibodies against this tissue are present in more than 90 percent of celiacs who are consuming gluten, yet they disappear quite rapidly
after excluding gluten. This form of blood testing was developed following recognition of the connection with celiac disease and demonstrates
that celiac disease is an autoimmune condition since these antibodies attack endomysium.
We have heard from patients who have had blood drawn for endomysium antibody testing for celiac disease while consuming a gluten-free
diet. Let us stop and consider this for a moment. While it is true that IgG
anti-gliadin antibodies will survive for six months or longer, endomysium
antibody tests are often used to check whether celiac patients are follow-
Testing for Gluten Sensitivity in All Its Forms
71
ing a gluten-free diet. If the endomysium antibodies are low or undetectable, the celiac patient is thought to be following the diet. How much
sense can it make to test for antibodies to identify celiac disease when the
patient is already following a gluten-free diet? This mistake can be terribly misleading and can have disastrous consequences.
This test is very sensitive, and it will identify 90 percent or more of
those patients with flat intestinal walls, but some evidence suggests that
it is less reliable for identifying cases with milder intestinal damage. Some
warn that reliance on blood testing alone will lead to missing a significant
number of cases of celiac disease. Perhaps, but there are some larger issues
to consider. Without this blood test, currently we would not be aware of
the startling frequency with which this disease is silently present in the
general population. Even granting that some cases will be missed by this
screening, when carefully conducted, endomysium antibodies are revealing a rate of celiac disease that is very close to 1 percent of the American
population.
When used in conjunction with IgG and IgA anti-gliadin antibody
testing, valuable information can be offered, thus allowing the patient to
make an informed choice about whether to continue to consume gluten.
The shift toward a heavy reliance on anti-gliadin antibody and EMA
blood tests has been under way in Europe for over a decade. It certainly
offers a huge improvement over the current situation, where only a tiny
fraction of celiac disease is ever diagnosed. Although a less than perfect
solution, it does offer some exciting possibilities, and as part of the growing arsenal of weapons against dietary gluten, we heartily endorse its use
when limited to case finding. However, a negative EMA blood test has
limited value for excluding celiac disease. This test is also limited by the
need for individual observation and evaluation of stained blood cells.
Tissue Transglutaminase (tTG) Antibody Testing
In the field of blood testing for celiac disease, the tissue transglutaminase (tTG) test is currently the newest entity. It is another step toward
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Dangerous Grains
solving the puzzle of celiac disease. Transglutaminase is an enzyme that
forms a normal part of endomysium and is involved in tissue repair. It is
the part of endomysium that anti-endomysium antibodies attack. Since
tTG antibodies can be identified by computer, it eliminates one of the
greatest weaknesses of EMA testing mentioned in the preceding paragraph.
The tTG test usually identifies about 98 percent of those who have
celiac disease, and it is a very specific test that can be used to rule out celiac
disease in about 95 percent of cases. This test appears to be superior to
endomysium antibody testing, not only because it is less costly but also
because it is a little better at identifying celiac disease and because interpretive bias is reduced by the use of computer scanning,
A New Development in the Offing
A tremendously convenient level of testing for celiac disease may
soon be available on the basis of this new development. A simple finger
stick and blood blot is all that is required for this new test, and results can
be available within an hour. It is expected to be commercially available in
the United States prior to the publication of this book.
RECTAL CHALLENGE
There is another exciting innovation for the diagnosis of celiac disease
that offers an answer to many of the current problems and testing errors.
A twentieth-century medical researcher who arrived in the twenty-first
century well ahead of most of us, Michael N. Marsh, M.D., has initiated
new directions in celiac research for this millennium. In addition to creating the standard by which well-informed pathologists throughout the
world evaluate intestinal biopsy samples for signs of celiac disease, Marsh
and his colleagues have also developed a test that is superior to the intestinal biopsy for identifying celiac disease. Known as a rectal challenge, it
Testing for Gluten Sensitivity in All Its Forms
73
is a procedure that can be conducted in the doctor's office using plastic
instruments, and clear, quantified results can be available in a matter
of hours.
As the name suggests, it is a procedure that first involves taking a
biopsy of the rectal mucosa. Then gluten slurry is placed into the biopsy
site, followed by a second biopsy from the same area four or more hours
later. Computer analysis of these tissue samples identifies immune reactions to gluten if they are present, thus leading to a diagnosis of celiac disease. While our description is somewhat oversimplified, the critical issue
is that this test differentiates those whose immune systems are sensitized
to gluten from those who do not react to it.
When the rectal challenge was first introduced in the late 1980s, it
was not well received. The most common objection was that it identifies
too many people as having celiac disease. Many authorities considered it
impossible that so many people could have this disease.
Since that time, innovative blood-testing methods such as EMA tests
and IgG, IgA, and tTG ELISA tests have dramatically increased the rate
at which celiac disease was diagnosed to the point where it is now found
in about 1 percent of the general population when it is sought. In ELISA
blood testing, a scanner is used to identify molecular complexes attacked
by endomysium antibodies and can be used to gauge the reaction of a
range of antibodies to gluten and to detect many food allergies. Therefore, the most common objection to the rectal challenge is therefore not
a legitimate one, as shown by the growing use of blood tests.
The second most common statement of resistance to this test is the
embarrassing nature of the entire procedure. The AGA, EMA, and tTG
ELISA tests are certainly more comfortable, convenient, and less invasive.
We can only acknowledge this criticism of the rectal challenge as valid
and recognize that this will deter many from seeking this test. The EMA
and tTG offer accurate, reproducible lab results but, when negative, do
not completely rule out gluten sensitivity or celiac disease. For those individuals with stout hearts and a willingness to undergo this procedure, it
can be very valuable.
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Dangerous Grains
Rectal Challenge Advantage
1. Unlike the intestinal biopsy, it identifies an immune reaction to
gluten and only gluten,
2. It costs much less than a biopsy.
3. It is a little more embarrassing but a lot less invasive than the
biopsy.
4. It reduces the risk of error-related patchy intestinal lesions.
5. It will not miss the milder cases of celiac disease that are missed
by blood testing alone.
6. It will reliably identify celiac disease for a full six months after
beginning a gluten-free diet, unlike any other test for celiac
disease.
7. The biopsies are analyzed by means of a computer. This eliminates the risk of human error due to variations in perception
from one person to the next, which is a problem in some types
of blood tests, as seen in jejunal biopsies and EMA.
8. The results are reported in a single numerical form, so their interpretation is infinitely less subjective and lend themselves to
standardization.
9. Patients can receive their test results much more rapidly, usually by the following day, although that will soon be overshadowed by the speed with which tTG test results can be made
available.
10. There is a reduced risk of complications due to the test. Although they are extremely rare in jejunal biopsies, the risk is
even smaller when taking a rectal biopsy, especially since only
one day's procedure is necessary for afirm diagnosis. This added
safety is especially important for infants, pregnant women, the
elderly, and the gravely ill.
Testing for Gluten Sensitivity in All Its Forms
75
SKIN BIOPSY, DERMATITIS
HERPETIFORMIS, AND IgA
DERMATOSIS
Dermatitis herpetiformis, a gluten-induced, extremely itchy, blistering
rash, has only recently been recognized as a subset ot celiac disease, although the debate of this issue appears to be subsiding. This offers another approach to obtaining an accurate diagnosis of celiac disease. If you
suffer from the gluten-induced skin lesions that are called either Duhring's
disease or dermatitis herpetiformis, a simple skin biopsy taken from uninvolved skin can provide a solid diagnosis. Most dermatologists will be
able to take a biopsy and send it for evaluation. The biopsy will reveal an
irregular layer of IgA deposited just below the basement membrane of
the skin. This will confirm the diagnosis of dermatitis herpetiformis and,
by implication, celiac disease.
Differentiation between dermatitis herpetiformis linear IgA dermatosis has, until very recently, been the only challenge. The pathologist could
confidently identify dermatitis herpetiformis where the microscopic view
of a layer of IgA antibodies, deposited just under the skin, was quite
rough and irregular. In linear IgA dermatosis, on the other hand, the layer
is quite regular and smooth in appearance.
In June 2001, however, one group of researchers reported a case of
linear IgA dermatosis in a patient who was also diagnosed with celiac disease. The skin disease, along with the associated celiac disease, responded
to a gluten-free diet and returned on gluten challenge. We would like to
see a variety of skin diseases similarly investigated.
GENETIC TESTING
If you or your family members have a genetic susceptibility to celiac disease, it can now be easily identified. Commercial blood tests are increasingly being used to identify genetic markers on wrhite blood cells, such as
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Dangerous Grains
HLA-DQ2, HLA-DQ8, and HLA-B8, all of which are found more frequently in those with celiac disease than in the general population. The
argument can legitimately be made that a greater number of people with
these genetic markers do not have and will never develop celiac disease.
However, it is reasonable and prudent to use such markers as guides to
suggest the possibility of celiac disease, thus raising the level of suspicion
for celiac disease for these individuals while significantly reducing the
number of individuals who turn out to have negative biopsies.
DIAGNOSIS AND LIFELONG
GLUTEN-FREE DIET
The process leading to a diagnosis of gluten sensitivity, celiac disease, or
dermatitis herpetiformis is often very trying. The testing choices we make
will also shape how we deal with the results. We recommend strict compliance with a gluten-free diet for everyone who tests positive for any of
the diagnostic tests, as well as for those close relatives of celiac patients
who have the genetic markers for celiac disease. We also recommend several other forms of testing and careful monitoring for additional illnesses.
The next chapter explains the diet and important follow-up testing.
mm
Life After Gluten
F
inally, you have a diagnosis—one you can use to improve or rebuild
your life. Regardless of the gluten-induced health hazards you wish to
avoid or the health problems you want to correct, the starting place is a
gluten-free diet. If you're new at this, you will quickly find that a glutenfree diet is not just a case of eliminating bread, breakfast cereals, and
pasta. Gluten grains and the countless foods and recipes made from them
permeate and shape our entire culture. The comfort they provide has
caused some of their widespread seductive, almost sensual appeal, which
also makes them difficult to give up. Throughout this chapter we provide
information about how to reduce the stress of the transition to a glutenfree lifestyle.
Adoption of a gluten-free lifestyle offers many rewards to those who
are willing to meet this important challenge.
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DEALING W I T H PHYSICAL
ADDICTION TO GLUTEN
The addictive nature of gluten is often overlooked. For some, the first
days and weeks of following a gluten-free diet are characterized by food
cravings, disorientation, irritability, sleepiness, depression, mental fogginess, fatigue, and/or shortness of breath, if you are a member of this group,
the very fact that you are experiencing many of these symptoms should
reinforce the need to exclude gluten from your diet. These are common
symptoms of withdrawal or detoxification from gluten-derived opioids
and brain neurochemical imbalances. The evidence suggests that about
70 percent of celiac patients will experience these symptoms when beginning a strict gluten-free diet.
We have stressed the need, when a gluten-free diet is indicated, for
strict avoidance ol all traces of gluten. There are several good reasons for
this strident recommendation. Ask anyone who has managed to break an
addiction and they will likely tell you that one of the secrets of their success is that they haven't "cheated" with small amounts on special occasions or at a weak moment. Such cheating actually keeps the addiction
alive or restarts it. The previously addicted ex-smoker and the alcoholic
ex-drinker will often state that they are one cigarette or one drink away
from starting their addiction again. They are often quite vigilant about
that first, apparently minor, slip because it is the one that begins their
slippery slide back into addictive behavior.
Most individuals who have celiac disease or non-celiac gluten sensitivity are also addicted to gluten.The morphine-like peptides from gluten
frequently stay intact because the bonds between some sequences of
amino acids are quite resistant to digestion. Those who have a leaky gut
will allow these opioids and other large peptides to enter the bloodstream.
The addictive process has probably been at work in most glut en-sensitive
and celiac individuals for many years, probably since childhood. This
makes elimination of gluten a great deal more challenging than might be
Life After Gluten
79
expected. It certainly requires more than a halfhearted suggestion from a
family doctor or gastroenterologist.
INFORMED AFTERCARE
Counseling
The counseling that was too often recommended as the only response
to legitimate symptoms of gluten sensitivity and celiac disease may now
have some value. As with any other addiction, its successful resolution will
often require a systematic, well-considered approach. Many support groups
provide the necessary contact with others who have gone through the same
experiences, or some people may require the intervention of addictionology health professionals who are versed in the treatment of addictions.
Dietary exclusion of gluten not only involves battling the physical and
psychological facets of this experience but also requires coming to terms
with the socially excluding nature of this diet. Few social occasions do not
include food and drink. Where gluten-free alternatives exist, the risk of
contamination is quite large. Even the beverages must be considered with
caution. This often decrees social isolation and a reluctant avoidance of
all social functions by the gluten sensitive.
Another important problem arises when gluten sensitivity is trivialized. Gluten-sensitive and celiac patients need to be given the necessary
support and guidance for breaking their addiction. They also need to be
carefully monitored. Where appropriate, most will also need to be tested
and treated for the health problems that developed as a result of their
prior gluten-consuming lifestyle.
Join a Celiac Support Group
We urge you to join a support group. Fortunately, there are many hundreds of them, with more sprouting up around the world every day. Take
a moment to visit the Internet to search for support groups in your area.
Dangerous Grains
Support groups usually produce informative newsletters that provide information on sources and identities of gluten-free foods, product safety,
how to stay truly gluten-free, and ingredient changes by particular manufacturers. The social events provide opportunities for members to share
experiences, recipes, and new information on a wide range of topics that
are relevant to those pursuing a gluten-free lifestyle. The counseling provided by the more seasoned members can sometimes be invaluable to the
newcomers, and the shared sense of community can be valuable to all.
A Gluten-Free Household
If you have a newly diagnosed celiac in your family, there are several
good reasons to implement a gluten-free household. First and foremost,
gluten sensitivity and celiac disease run in the family. Not only will it certainly be a safer environment for the celiac/gluten-sensitive individual,
but it will also help other family members develop a better understanding of the challenges faced by the gluten-sensitive family member. And
it will ensure an improved diet for the entire household, which may lead
to some unforeseen health improvements for other family members.
A gluten-free environment can also reduce the workload for the family
cook by allowing the preparation of a single meal for all.
Testing for Additional Food Allergies
Additional food allergies are the rule among the gluten sensitive. Testing for common food allergies such as milk, soy, and eggs is a critical part
of the program for regaining health after identification of a problem with
gluten. IgG ELISA blood testing for delayed food allergies is our current
recommendation.
Bone-Density Testing
Seventy percent of all undetected celiacs have significant bone loss.
That being the case, bone-density testing should be conducted annually.
Life After Gluten
81
This will ensure that the diet and appropriate supplementary bone nutrients are effectively reversing the damage previously done by gluten. This
regular testing is particularly important because of the current preoccupation with calcium supplementation at high doses for those with compromised bone-mineral density. To date, the published research that shows
the most promise for remineralizing bones in celiac patients—beyond
simply following a strict gluten-free diet—clearly favors magnesium and
zinc, as well as vitamins D and K supplementation.
Regular Thyroid Testing
Laboratory testing for thyroid function is usually limited to blood tests
that look closely at the thyroid-stimulating hormone (TSH) and free T4.
Under usual circumstances, this is perfectly appropriate. However, given
the high rate of autoimmune thyroid disease among the gluten-sensitive,
more extensive testing is warranted in any gluten-sensitive individual and
his or her immediate family members. Regular testing should also include
monitoring blood levels of triiodothyronine and thyroxine (T3) along with
anti-thyroid antibodies to ensure that any gluten-induced autoimmune
thyroid problems are identified early. Early detection and a subsequent
gluten-free diet have been reported to reverse autoimmune thyroid disease.
Glucose-Tolerance Testing
Appropriate testing should also be conducted in response to the risk
of hyperglycemia (high blood sugar) and Type I diabetes, which is substantial among those who are gluten sensitive. First-degree family members of known gluten-sensitive individuals should also be monitored for
Type I diabetes along with celiac disease.
Liver-Function Testing
Liver function should also be watched carefully in the gluten sensitive. Some liver enzymes will often be quite abnormal at the time of diagnosis. In many cases, this will soon normalize on a gluten-free diet. We
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believe it is important to be aware of this inclination if you are one of the
gluten-sensitive individuals whose liver reacts abnormally to gluten. Such
insights probably do not warrant a gluten challenge, so testing liver enzyme levels at the time of or shortly after, diagnosis will provide valuable
information.
Quarterly Eye Exams During the First Year
It may sound excessive to recommend such frequent eye exams, but
the headaches and discomfort caused by blurred vision are often quite
disruptive to one's life. Since many newly diagnosed celiacs experience
quite a lot of change during the first year or so, these checkups and consequent modifications of correction may help reduce the negative impact
of the changes and difficulties.
Dental Work
It is important to let your dentist know about your sensitivity to
gluten, because it can cause enamel defects such as horizontal and vertical grooves, as well as an increased frequency of dental caries. In addition,
chronic periodontal disease with unhealthy gums could possibly be the
result of your gluten sensitivity—not the result of poor oral hygiene, as
is often assumed. The gluten-free diet will often reverse this problem,
so minor interventions coupled with a "wait and see" approach may be
preferable to surgical interventions in gum disease associated with gluten
sensitivity.
NUTRITIONAL CAUTIONS
Once you are aware that you are gluten sensitive, it is also important to
avoid certain pitfalls.
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Desensitization Therapies
These procedures can be an effective means of reducing symptoms of
gluten sensitivity, celiac disease, and other allergies. Administering small
amounts of an allergic or toxic substance in an attempt to desensitize a
sensitized individual is the principle by which allergy shots work. They
may also work on the principle of adaptation that was described by Hans
Selye seventy years ago. However, such therapies, especially in the area of
powerful genetic predilections, as found in gluten sensitivity, risk the very
consequences that Selye also identified in his work so long ago. Early
death was the consistent result of adaptation to chronic physical stressors.
Premature death is the consequence of continued exposure to gluten in
the gluten sensitive.
In essence, desensitization therapies disarm the warning system provided by your body. By reacting to a given substance, your body is letting
you know, either with symptoms or with abnormal immune responses,
that this substance is not healthful. We suspect that such reactions have
developed through the evolutionary process. If foods or other substances
make us feel ill, and if we know which foods these are, we should—unless
the addictive cravings exceed self-discipline—avoid them. Those who do
not feel ill in response to allergic substances in their environment are
more likely to succumb to the harmful effects of these allergens. Thwarting this efficient, finely tuned system that warns us to avoid allergenic
foods is inappropriate.
Trace Quantities of Gluten
For the same reasons, taking a cavalier attitude toward consumption
of trace quantities of gluten can also prove to be hazardous. Regular ingestion of small amounts may create an adaptation to gluten that is similar
to that created by desensitization therapies. Through chronic ingestion of
trace quantities, a psychological perspective may develop. Given the addictive nature of gluten, maintenance of a mostly gluten-free diet risks
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either a chronic and unpleasant battle with addiction or the beginning of
a slippery slide back to regular gluten consumption.
Gluten Ingredients in Pharmaceutical Products
Recall that less than one gram of gluten daily is enough to perpetuate
a diseased intestinal lining. With this in mind, it should no longer seem a
petty issue that non-medicinal food ingredients in pills from the pharmacy can pose quite a challenge, especially for those who are acutely sensitive to gluten.
Many pharmaceutical companies have contracts with food suppliers
for starch-binding materials. Unless explicitly instructed otherwise, the
contractor will understandably choose the least expensive supplies. Sometimes that will mean that corn starch will be used. At other times, wheat
starch will be most cost efficient. The net result is that, unless a pharmaceutical manufacturer has specified the source of the starch binder in its
contract with the food supplier, you may be exposed daily to sensitizing
doses of gluten when taking your medication. Your pharmacist, doctor,
and manufacturer may not be able to say whether there are trace amounts
of gluten in the non-medical ingredients used to fill your prescription.
The best strategy is to ask your doctor to specify that the prescription is
open to substitution from a manufacturer that uses gluten-free binders.
Many do.
Steroids
Steroid medications, although valuable in certain instances, may pose
several important hazards to those who are gluten sensitive. Demineralization or thinning of our bones is already a major risk as the result of
years of gluten consumption. Steroid medications add to that risk as a
consequence of further worsening of a leaky gut, complicating bloodsugar regulation and demineralizing our bones. Many gluten-sensitive individuals have spent years battling intestinal, vaginal, and systemic fungal
infections as a direct consequence of steroid medications.
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85
With the exception of steroids needed to stabilize breathing in an asthma
attack, we urge extreme caution in the use of these drugs by those who are
gluten sensitive.
Dapsone
Although this leprosy medication is quite effective for reducing the
extreme itching associated with dermatitis herpetiformis lesions, high
doses have been shown to cause cancer in rats. Given the extraordinary
increased risk of cancers, the frequency of neurological disease, and the
overlap of the latter conditions among those with gluten sensitivity or
celiac disease, considerable caution seems in order. The best and safest
therapy for dermatitis herpetiformis remains strict avoidance of gluten.
OPTIMAL NUTRITION ON
A GLUTEN-FREE DIET
Following a gluten-free diet is not at all easy. Because it is a difficult diet
for most people to follow, it is especially challenging for the first six months
or so while you adjust your thinking, increase your knowledge, and develop the shopping and eating habits needed to be strictly gluten free.
In general, a gluten-free diet excludes all foods made from wheat, rye,
and barley. This prohibition includes avoidance of pastas, pancakes, batters, breads, and other baked foods, except where they are prepared with
flours made from rice, corn, nuts, amaranth, quinoa, and other gluten-free
foods. Appendix B provides a complete listing of unsafe sources of flour,
but there are a few important issues that need explanation.
Strict avoidance of gluten quickly leads to healing of the small intestinal lining and improved nutrient absorption. This can have some surprising implications that require cautious implementation of the best
dietary practices. In today's high-pressure world of tight time lines and
fast food, it is no small task to consistently eat a healthy, well-rounded
diet. In general, we recommend that, wherever possible, meals should
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consist of a wide variety of fresh meat, internal organs, poultry,fish, fruit,
vegetables, and antioxidant herbs and spices.
Eat whole, unprocessed, and organically grown food when possible.
Like unprocessed foods, organically grown food has fewer man-made
chemicals and toxic metals, and often has a higher nutrient content, including improved protein quality and up to 30 percent more vitamin C,
iron, magnesium, and phosphorus.
We also recommend five to nine servings of a wide variety of nonallergenic fruits and vegetables each day. The more vegetables and fruits
one eats each day, the less likely he will develop food allergies and intolerances. Such healthy eating habits will reduce inflammatory disease
and result in fewer heart attacks, strokes, and cancers, and overall better
health.
A healthy diet of fruits and vegetables should include one bountiful,
mixed salad daily with extra-virgin olive oil, flaxseed oil, or an essential
fatty acid oil blend. Quercetin-ricn foods such as apples, red and yellow
onions, chives, and all kinds of berries are strongly recommended. Also, be
sure to include the many excellent detoxifying cruciferous vegetables
such as broccoli, cauliflower, brussel sprouts, kale, cabbage, watercress,
kohlrabi, and bok choy.
In addition to a daily broad-spectrum multi-vitamin/mineral, we recommend that you supplement with extra vitamin C and natural, mixed
vitamin E and carotenoids. Frequent use of antioxidant, anti-inflammatory
culinary spices such as fresh garlic, ginger, and turmeric (Indian curry), as
well as herbs such as oregano, dill, thyme, and sage in your food preparations is also extremely valuable.
Fats and Oils
Repeated high-temperature heating of oils and fats converts them to
pro-inflammatory, cancer-causing substances, so fried foods need to be
strictly avoided. Lower-temperature steaming, boiling, broiling, stir-frying,
and roasting are preferable to frying. It is particularly important to avoid
all hydrogenated fats, oils, and margarines. The evidence indicates that
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87
when eaten in excess, these man-made oils, found in many processed
foods, behave as pro-inflammatory, carcinogenic substances in our bodies.
Be cautious about pursuing a low-cholesterol diet. Extremely lowserum cholesterol (under 160 mg/dL] is associated with an increased risk
of strokes, cancer, sudden death, and suicide. Instead of following such a
diet, we recommend that you increase your consumption of a blend of essential fatty acids every day. These include liberal amounts of omega-3
fatty acids (fish oil, flaxseed oil, and walnut oil, e.g.), omega-9 fatty acid
(extra-virgin olive oil), and a more limited intake of omega-6 oils (vegetable and seed oils) and arachidonic acid (animal fat), including the yolk
from boiled and poached eggs.
Animal Protein
Eat four- to six-ounce servings of fresh, unbreaded, unfried, oily, nonalleTgenic fish two to five times a week (salmon, Alaskan halibut, orange
roughy, sardines, Chilean sea bass, trout, and mackerel, e.g.). Large fish
such as shark and swordfish are reported to contain high concentrations
of mercury and should therefore be avoided. Weekly servings of shellfish,
such as shrimp, crab, and lobster, can be very beneficial. Yet, you should
be aware that shellfish are common allergens and may also accumulate
pollutants.
We suggest eating lean red meat, boiled or poached eggs fortified with
vitamin E and omega-3 oils, and omega-3 oil-rich wild game such as deer,
elk, buffalo, and/or rabbit once or twice a week. In addition to being free
of antibiotics and growth hormones, these meats add another important
element to the diet by broadening the range of dietary proteins. Wild
duck, goose, pheasant, and quail also provide many of the same advantages, including variety Domestic poultry is also a healthful option when
it has been range-fed and has not been treated with growth hormones
and antibiotics.
Internal animal organs such as liver, heart, pancreas, and bone marrow
should be part of our weekly diet as well. For hundreds of thousands of
years our ancestors ate not only an abundance of wild game, fish, and
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shellfish when available but also appear to have preferred internal organs
to muscle meat when the luxury presented itself
Caution about Substituting for Gluten
It is important to establish eating habits that will ensure you get the
greatest possible benefits from your gluten-free, allergen-free diet. For instance, gluten-free substitutes for treats such as cakes, cookies, pastries,
and breads are much more calorie-dense than their gluten-containing
counterparts. Underweight, newly diagnosed individuals who are in the
habit of consuming large quantities of food may now be at risk of excessive weight gain because their absorptive capacities have increased dramatically, and these substitutes are so much richer in empty calories,
causing abnormal spikes in blood insulin and sugar levels.
Newly diagnosed teenagers are particularly at risk for this increase in
blood-sugar levels. The conventional adolescent diet in our culture is
laden with foods such as rice, corn, potatoes, refined sugars, gluten-free
snacks, and soda. Although these foods are gluten free, habitual overindulgence elevates blood insulin and sugar abnormally, often resulting in
obesity, high blood pressure, elevated blood fats, non-insulin dependent
diabetes, and heart disease.
Additional Food Sensitivities
There are frequent reports of celiac patients continuing to suffer from
chronic symptoms while following a strict gluten-free diet. Milk, soy,
corn, egg, and other delayed-onset food sensitivities are commonplace
among celiac and gluten-sensitive patients. With the elimination of offending foods, many lingering symptoms improve or disappear.
Remember that those who are gluten sensitive are also likely to have
multiple delayed-onset food allergies, with dairy products heading the list
along with corn, soy, eggs, citrus fruits, and seafood. Peanuts and/or yeast
are also common allergens, IgG ELISA allergy testing is an important
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89
laboratory tool for identifying these hidden allergens and subsequently
developing a healthy diet. Once allergic foods have been properly identified, a two- to four-day rotation diet should be planned. A wide variety of
non-allergenic foods will help build a healthier body.
Beverages
Alcoholic beverages should be avoided during the first three to six
months of healing. Alcohol causes or worsens a leaky gut, thereby perpetuating illness and delaying recovery. Also, in addition to eliminating
soda from your diet, we recommend that you do not exceed two cups of
decaffeinated or regular coffee each day. Consider replacing coffee with
green or black tea. It is important to drink eight to twelve glasses of
filtered water daily (roughly one ounce of water for every two pounds
of body weight). Avoid tap and well water, if possible. Be cautious
about substituting fruit juice for water or fresh whole fruits. Reports of
weight gain and retardation of vertical growth in children have been reported.
Other Recommendations
Consume foods and beverages that are high in the anti-allergy, antiinflammatory, antioxidant bioflavonoid quercetin; these include apples,
green and black teas (but not coffee), red and yellow onions (but not white
onions), and red wine (but not white wine or beer). High quercetin dietary
intake reduces the risk of premature death from all common causes.
A Day in the Life of the Gluten Free
You may want further clarification regarding how you can structure
each day's gluten-free meals. Here is an illustrative example of such a
diet, excluding allergenic foods on an individual basis:
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BREAKFAST
a cut of lean meat and/or I to 2 boiled or poached eggs fortified
vitamin E and omega-3 oils
fresh fruit
with extra
a slice of gluten-free toast or a rice cake with jam
a cup of tea
LUNCH
mixed vegetable soup made with plenty of bones
or
Fresh steamed, broiled, or baked fish
or
shellfish with a bountiful mixed salad, vegetables, and a fresh-fruit
EVENING
cup
MEAL
....
as potatoes, whole-grain rice, or gluten-
free pasta
steamed or raw mix of vegetables
SNACKS
celery or carrot sticks
pickles
pickled herring
olives
nuts and seeds
OCCASIONAL TREATS THAT
HAVE A VERY H I G H
(caution is required)
popcorn
corn or taco chips
potato chips
french fries
gluten-free rice cake, cookies, pastries, etc.
sesame snaps
GLYCEMIC
INDEX
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The Rotation Diet
Eating favorite foods every day, even eating from the same food group
day after day, is a recipe for developing food allergies. This is especially
true for those who are gluten sensitive because of their propensity for a
leaky gut. When the gut is leaky, a certain amount of food protein will
be absorbed into the bloodstream. If this occurs daily, or several times a
day, the immune system is bound to become sensitized to it and begin to
mount an immune response to it. Remember, it is the foreign proteins in
microbes that your immune system recognizes and reacts to. Any foreign
proteins, including those from foods that arrive in the bloodstream in
any quantity, are likely to spark an immune response. That likelihood increases with daily or more frequent exposure.
We recommend that after eating a particular food, you avoid that food
group for two days. This is called rotating your foods, or a rotation diet.
If you eat potatoes on Monday, for instance, you should avoid that
food until Thursday. It can be a bit of a chore to keep track of all these
food issues, but the benefits will soon encourage your continuation of a
rotation diet. One important tool for following a rotation diet is a food
diary. Just as you might keep a daily appointment book, you would simply record all the foods you eat each day.
Rotation not only reduces the risk of developing further food allergies
but also forces you to eat a wider variety of unprocessed, unpackaged, less
chemically laden foods, which is also an important strategy for achieving
optimal health. The food diary reinforces such healthy eating habits.
Eating Gluten-Free Away from Home
As with the person who carries cards that provide a convenient means
of making contact to conduct business, you may wish to carry a card that
provides appropriate information to restaurant employees. Restaurant cards
can be printed in the same format as a business card. An example of such
a card is provided below:
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Dangerous Grains
I N E E D Y O U R HELP. 1 B E C O M E VERY S I C K W H E N I EAT G L U T E N G R A I N S .
Hence, I follow a gluten-free diet, I need to avoid all forms of wheat, rye,
oats, barley, triticale, spelt, and kanaut This includes all malt, TVP, TPP,
HVP, HPP, and MSG. Unless it is clear that they do not come from one of
the above grains, I must also avoid all vegetable starch, food starch, and
natural flavors.
Thank you for your assistance and cooperation.
Our experience with restaurants has been very positive. We find that
most are quite happy to help and are usually quite successful in preparing gluten-free meals.
DIETARY SUPPLEMENTS
Some fats are absolutely essential to humans. We cannot maintain good
health without them, yet our bodies are unable to synthesize them. Cereals are very low in omega-3 essential fatty acids. Substituting other cereals for gluten grains is a step in the right direction, but this approach
continues to displace dietary meat and other sources of omega-3 fatty
acids and further compromises one's nutritional well-being. We must get
these fats from our diets or supplements.
Eight amino acids are equally essential to human health and must come
from our food supply. Some essential vitamins are abundantly available in
animal products, such as vitamin B 12 , yet they are not found in other food
sources, including gluten cereals. We humans are members of a very select animal group. Guinea pigs and humans are the only mammals that
cannot synthesize their own vitamin C. Hence we are also the only animals at risk of developing scurvy. Cereal grains contain very little of this
health-promoting vitamin. By displacing fruits and vegetables, the consumption of cereals reduces our vitamin C intake.
All of these factors combine to counter the current high complex car-
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93
bohydrate, high dietary gluten-grain fad. Our cells can utilize carbohydrates for energy, but they can also use fats. The difference is that there
are some fats that we must get in our diet (called essential fatty acids)
while there are no known essential carbohydrates.
A properly prepared animal protein-dominated, low-cereal diet that
includes plenty of fruits, vegetables, nuts, and seeds offers us the nutrients
essential to our good health. Failure to absorb these nutrients, and the absence of other critical nutrients from these cereal-derived foods, has created many of the nutritional deficiencies that plague our culture, despite
our calorie-rich lifestyles.
Nutrient absorption is so variable, even in treated celiacs, that individual assessment, leading to individually tailored advice, is the best approach. Depending on which part of the intestine is injured, the extent of
the damage, how often accidental ingestion occurs (for instance, those
who do a lot of traveling would be at greater risk), and how long the damage persists, there can be quite a variation in need for a particular supplement. Although a complicated issue, supplementation is very important
to achieving optimal health; therefore, gluten-sensitive individuals should
pay considerable attention to this important issue. Regular monitoring of
blood levels of vitamins and minerals is an important first step. During
the first year, monthly or bimonthly monitoring offers a means of checking for deficiencies, as well as monitoring the impact of supplementation.
Magnesium Supplementation
Magnesium is essential for proper maintenance of the parathyroid
gland. Not only is this gland a major regulating factor in your body's calcium metabolism, but endomysium antibodies have also been shown to
cross-react with the tissues of this gland. That means that many individuals with celiac disease will derive important benefits from magnesium
supplementation. We can only speculate that similar benefits might be
derived by many of those who are gluten sensitive. Magnesium deficiency
may play a key role in many of the common symptoms and medical conditions overrepresented in untreated celiacs and gluten-sensitive individ-
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ualfi, including osteoporosis, migraine headaches, muscle pain or spasms,
major depression, chronic fatigue, premenstrual syndrome, asthma, autism,
heart disease (cardiomyopathies] in children, and seizures.
Magnesium supplementation over a two-year period results in a raised
serum parathyroid hormone and improved bone density.
The impact of magnesium supplementation is an excellent example
of the need to tailor recommendations to the gluten sensitive on an individual basis. Based on clinical improvements, there can be little doubt
that gluten-sensitive individuals are almost universally deficient in this
important mineral. However, magnesium levels are very difficult to measure accurately, so it is probably more useful to monitor the many functions
that improve as a result of magnesium supplementation. For instance, improvements in bone density and parathyroid hormone levels in the blood
can both be good indicators that magnesium supplements are providing
benefits. Reduction or disappearance of bone pains, muscle twitching,
and an inclination to muscle cramping can all indicate the value of supplementing magnesium.
This important mineral also loosens the bowels. This can be a real
blessing for those gluten-sensitive individuals who struggle with constipation, but it requires caution and careful attention from those who are
inclined to diarrhea.
Calcium Supplementation
Calcium supplements are taken by individuals who are unable to get
enough calcium in their regular diet or who have a need for more calcium,
such as growing children, postmenopausal women, the elderly, pregnant
or breast-feeding women, and many celiacs. Supplements are used to
prevent or treat several conditions that may cause hypocalcemia (not
enough calcium in the blood). The body needs calcium to make strong
bones. Calcium is also needed for the heart, muscles, and nervous system
to work properly Given almost universal bone mineral depletion in
adult-diagnosed celiacs, calcium supplements are extremely likely to be
recommended. We remind the reader that bone health and density de-
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pend on multiple factors and nutrients, including but not limited to magnesium, zinc, boron, vitamin D, and vitamin K, in addition to calcium.
However, excessive calcium supplementation at the expense or avoidance of other key bone nutrients can lead to several problems for those
who are gluten sensitive. High intakes of calcium supplements may interfere with the absorption of other nutrients such as iron and zinc. Intake of calcium supplements may also interfere with the absorption of
concurrently consumed medications, and vice versa. Other potential adverse effects of chronic intakes of high doses of calcium include milkalkali syndrome (ectopic calcium deposition) and hypervitaminosis (i.e.,
in the case of supplements containing calcium and vitamin D).
Further, calcium and magnesium share the same transport mechanism
for absorption across the intestinal barrier. Excessive calcium supplementation may overwhelm this mechanism, inhibiting the absorption of magnesium, thereby aggravating a preexisting magnesium deficiency or inducing
a magnesium deficiency where it might not otherwise occur. Magnesium
has also been identified as a common cause of osteoporosis in celiacs,
even on a gluten-free diet. Some researchers have found evidence for a
ratio of 1:1 in hunter-gatherer diets, suggesting a similar ratio for supplementation of calcium and magnesium.
Selenium Supplementation
Selenium is a mineral that is used to treat some skin diseases, and
small-quantity supplementation has been shown to reduce the risk of some
cancers. Selenium deficiency is common in non-celiac gluten-sensitive
patients and untreated celiacs. Selenium deficiency continues to be one
of the conditions commonly overrepresented in the gluten sensitive, leading to the risk of developing many other conditions such as proneness to
esophageal and other cancers, heart disease in the form of cardiomyopathy, infertility, miscarriages, kidney disease, chronic liver disease, asthma,
underactive thyroid, testosterone deficiency (selenium is required for
production of both thyroid and testosterone hormones), Down syndrome,
autism, and accelerated death from AIDS (selenium deficiency increases
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Dangerous Grains
the death rate from AIDS by twentyfold!}. Given the increased risk of
cancer and premature death among the gluten sensitive, selenium supplementation can be used to counter both the limitations imposed by
malabsorption and poor diets alone and the limitations caused by selenium depletion in the soil of some farming regions.
Iron Supplementation—A Word of Caution
There can be little doubt that iron deficiency is an important, widespread problem in gluten sensitivity. Often, simply by eliminating gluten
from the diet, the problem is solved. On the other hand, additional iron
as an iron supplement can be very important for establishing and maintaining optimal health in those with persistent iron deficiency. It is extremely important to identify iron deficiency early in an infant and young
child's life because chronic iron deficiency is thought to be associated
with permanent loss in intelligence, school performance, and other cognitive abilities. Be aware also that vitamin B ] 2 deficiency coexists in about
15 percent of children with iron deficiency and that cow's milk allergy is
another extremely common cause of blood-loss iron deficiency in children. All these factors have to be monitored and effectively treated.
Common symptoms of iron deficiency may include pale complexion,
pale fingernail beds, rapid heartbeat, chronic fatigue, easy bruising, excessive nose bleeds (this may also indicate a vitamin K deficiency, commonly
found in celiacs), diminished exercise endurance or tolerance, indigestion, difficulty swallowing, loss of taste, symptoms of "restless leg syndrome" (creepy, crawly sensations in legs, relieved by movement of the
legs—magnesium is helpful here, too), heartburn, chest pain, anxiety or
depression, and attention and/or learning deficits in children.
Be aware that you don't want to supplement with iron unless you
need it. Excess iron can pose a hazard to men, postmenopausal women,
those who frequently eat red meat, and those who regularly supplement
with large doses of vitamin C (over 500 to 1,000 mg daily). Iron supplementation should be managed in collaboration with your doctor on the
basis of regular blood tests that have confirmed existing iron deficiency.
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To repeat, do not take iron supplements unless you need them. Excessive
iron can cause potentially life-threatening damage to the heart, liver, and
pancreas.
Potassium Supplementation
Potassium deficiency is associated with irregular heartbeat, salt-sensitive
high blood pressure, enlarged kidneys, kidney failure, recurring kidney
stones, and fatal strokes. Commonly, chronic diarrhea is the underlying
cause. Therefore, potassium is another mineral that should be closely
monitored. Normally, a gluten-free diet with lots of fresh fruits, vegetables, lean meat, fish, and poultry will supply you with all the potassium
you need. On occasion the diet proves inadequate in supplying potassium, and supplementation should be considered after collaboration with
your doctor. Potassium deficiency, in association with muscle wasting,
weakness, and paralysis, has been reported in celiac disease.
One note of importance: Magnesium and potassium deficiencies often
coexist in celiac disease. If you have persistently low serum potassium
levels, not corrected with proper diet or supplementation, more magnesium supplementation is frequently needed. If low magnesium and potassium levels coexist, magnesium supplementation will often bring both
the magnesium and potassium levels back to normal values.
B Vitamin Supplementation
B vitamin deficiencies are common in gluten-sensitive individuals and
those with celiac disease. Folate, B p , and B 6 deficiencies are of special importance due to their relationship with neural tube defects in newborns,
seizure activity, and increased risk of heart attacks, strokes, and cancer associated with elevated blood levels of homocysteine. Vitamin B (j deficiency has also been reported to play a role in carpal tunnel syndrome,
major depression with fatigue, asthma, PMS, attention deficit disorder,
and the nausea and vomiting experienced during pregnancy.
When our absorptive capacity is compromised by gluten, it is difficult
Dangerous Grains
to predict which of these B vitamins, and in what quantity, we should
supplement. Because we excrete any excess that we do not need, conventional wisdom suggests oversupplementation, trusting urinary excretion for maintenance of optimal levels.
We are aware of at least one report of nerve injury as the result of excessive vitamin B s supplementation in excess of 150 mg daily. We recommend exercising caution when supplementing with this B vitamin.
For those with chronically low blood pressure, a common feature of
celiac disease, caution is also appropriate when supplementing with vitamin B 3 . Some individuals choose to begin with very small doses.
Vitamin A Supplementation
Vitamin A deficiency is commonly associated with recurring infections, especially in children. Vitamin A deficiency is also the leading cause
of blindness in children worldwide. The ability to safely take vaccinations
also appears to be closely linked to vitamin A status. Deficiency of zinc
and this vitamin may also play a key role in food allergies.
Although vitamin A deficiency is often a problem in gluten sensitivity,
it is not safe to oversupplement. Excess vitamin A has been observed to
cause headaches and dry skin. More critically, doses in excess of 10,000 IU
daily may cause birth defects. Much higher sustained doses can have a devastating impact on your own health and, in rare instances, may be fatal.
Vitamin A supplementation should not be undertaken carelessly.
Collaboration with your doctor and regular testing are critical parts of
your program for supplementing with this vitamin if you show signs
of deficiency.
Vitamin E Supplementation
Vitamin E deficiency, perhaps in conjunction with selenium deficiency,
may be associated with accelerated heart disease, strokes, Alzheimer's
disease, Parkinson's disease, diabetes, cataracts, and prostate cancer. One
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or more of the fat-soluble vitamins, vitamin E included, have been reported to be deficient in celiacs. However, caution is also important in
taking vitamin E supplementation. These vitamins are stored in body fat,
and toxic accumulations may occur.
Vitamin D Supplementation
Vitamin D deficiency is thought to be a causative factor in osteoporosis, osteomalacia, psychological depression, suicide, and colon cancer.
Low blood and tissue levels have been reported in untreated celiacs.
The safest, cheapest source of this vitamin is exposure to sunlight.
However, with mounting concerns about skin cancer, this source of vitamin D has lost some of its appeal. Those institutionalized in hospitals and
nursing homes, those living at more northerly latitudes, and those who
work long hours inside are even less likely to get adequate vitamin D
from the sun. Vitamin D supplementation has now become the norm.
DIETARY DANGERS
Oats: To Eat or Not to Eat, That Is the Question
The inclusion of gluten-containing oats remains a bit of a hot topic
among those who follow a gluten-free diet. Oats advocates point to current studies showing no change in shape or size of the intestinal villi of
celiac patients. Since the gliadin proteins that cause damage to the intestinal villi have been identified and are not present in oats, oat advocates
consider them safe to include in the gluten-free diet. Many also argue for
including oats because they believe that it will provide a valuable substitute for some of the missing foods made from wheat, rye, and barley, thus
making the diet more tolerable.
Conversely, those who wish to see oats continue to be excluded from
a gluten-free diet argue that, because oats are handled with the same
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farm machinery and stored and milled in the same facilities as the other
three gliadin-rich grains, gliadin contamination is inevitable.
Further, while it is true that the proteins that cause villous atrophy are
not present in oats, opponents argue that all other gluten proteins in this
grain have not been proven harmless. In fact, glutenin, another gluten protein, is currently receiving a lot of attention in the research community as
the protein associated with asthma and autoimmune skin conditions.
Oats also cause abnormal changes to white blood cells inside a test
tube, and, most important, many celiacs develop symptoms in response
to oats. This may result from immune responses that cause increased intestinal permeability or other negative health consequences.
We have already established that there are many more cases of nonceliac gluten sensitivity where there is a leaky gut in the absence of villous atrophy than cases of celiac disease. It is not yet clear whether any of
the gliadin proteins identified as causing damage to the villi are also causing intestinal permeability in the non-celiac gluten sensitive. If the same
proteins are simply causing a different form of damage to the intestinal
wall, the distinction between gluten sensitivity and celiac disease becomes
even more blurred. If there are non-gliadin proteins in gluten that cause
a leaky gut in those who are gluten sensitive, they might also be causing
increased intestinal permeability in celiac patients.
DON'T
EAT
OATS!
Given the evidence, we advocate excluding oats until there is clear evidence of its safety by demonstrating that all proteins from this grain do
not cause either intestinal permeability or any other form of damage to
the gastrointestinal tract or elsewhere.
Wheat Starch
There are thoughtful arguments on both sides of the wheat starch
debate as well. When tested, celiacs consuming wheat starch as part of
an otherwise gluten-free diet do not show intestinal damage or suggestive antibodies in the blood. Wheat starch advocates claim that since
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wheat starch is often tolerated by very sensitive celiacs, it is likely harmless, at least for those who do not react to it. In England, where the
gluten free diet has been shown to reduce the risk of cancer and other
sequels of untreated celiac disease, wheat starch has long been accepted
as gluten free.
We hasten to point out that a failure to react or a lack of observable
intestinal damage do not guarantee that gluten is not causing harm. Furthermore, given the rate of asymptomatic silent celiac disease, the use of
symptoms as evidence of sensitivity is highly questionable when evaluating the safety of wheat starch. Intestinal biopsies also fall far short of that
perfection when used to identify low levels of gluten consumption due,
in part, to the frequency of patchy damage to the intestinal wall. This also
applies to the blood tests for celiac disease, especially when performed as
single tests on people who are consuming only small amounts of gluten.
The exception to this rule may be when EMA and tTG celiac tests are
combined—a 94 percent sensitivity has been reported for those consuming wheat starch.
don't
EAT W H E A T
STARCH!
To add to the wheat starch confusion, there are two current studies
that provide evidence in support of opposing sides of the argument. We
take the position that claims for the safety of certain foods should be
based on firm evidence. The purification process that separates wheat
starch from gluten protein is not a perfect one. In the absence of a preponderance of evidence to the contrary, we err on the side of caution by
recommending against the consumption of wheat starch.
Additives
Developing the habit of relentlessly reading ingredients lists on labels
is a critical part of successfully following a gluten-free diet. Rule of thumb:
Any processed food is suspect. In addition to avoiding wheat, rye, barley,
triticale, spelt, kamut, malt, and oats, it is also important to be on the alert
for the acronyms that can spell trouble-. HPP, HVP, MSG, TPP, and TVP
102
Dangerous Grains
Acronyms That Might Spell "Hidden" Gluten
1
• 1' I
Fu—dried wheat gluten
HPP—hydrolyzed plant protei
HVP—hydrolyzed vegetable p rotein
MSG—monosodium glutamat<a
TPP—textured plant protein
TVP—textured vegetable prot sin
(see the box above, where we spell out the words from this alphabet
soup). While these substances may not be refined from gluten, there is a
good chance that is exactly where they come from. Vegetable starch, food
starch, modified food starch, and natural flavors should also be avoided,
as the source of these additives is difficult to determine.
There are good financial reasons that food manufacturers use these
generic terms and acronyms to identify constituents of their products.
This practice allows them to switch supply sources of these ingredients
according to daily price changes or other market considerations, without
the expense of changing their labels each time. Only when informed consumers pressure for changes in such practices will we see specific labeling
with the full name of the ingredient on the label.
Other Hidden Hazards
Throughout the industrial world, laws governing food labeling allow
manufacturers considerable latitude. The scientific reality is that trace
quantities of gluten and other allergenic substances are difficult to identify. A United Nations commission operating under the auspices of the
FAO and WHO sets the standards for food labeling and is called Codex
Alirnentarius. This commission has established minimum levels of gluten
content that are allowed in foods labeled "gluten free." This may seem
Life After Gluten
10
contradictory, even foolish, but it is a reality that has shaped labeling legislation throughout the world.
Closer examination reveals some reasonable arguments in favor of this
perspective, if only because it is extremely difficult to identify and measure very small quantities of such gluten contamination, which would
make more stringent legislation difficult or impossible to enforce. In many
parts of Europe, where wheat starch has long been accepted as gluten free,
this perspective may not raise eyebrows. However, the support groups in
the United States, Canada, New Zealand, and Australia have long advocated a policy of zero tolerance.
At a recent international conference in Tampere, Finland, many visiting
gluten-sensitive delegates from these zero gluten tolerance countries found
themselves suddenly erupting with dermatitis herpetiformis lesions. This
could have been the result of some other form of contamination, as they
were presumably eating in restaurants most or all of the time. Conversely,
it could have been the result of eating foods that contained wheat starch
and oats, which form part of the "gluten-free" diet in these countries.
Due to the undeniably high prevalence of gluten sensitivity and the
extraordinarily small amounts of gluten capable of mischief, we strongly
encourage labeling that reflects the true nature of the contents of the
food in question. If a food product is truly gluten free, we would want the
labeling to reflect that. If, on the other hand, solid scientific evidence
comes to light suggesting that some reduced level of gluten is permissible, we would expect the labeling to read something like "low gluten" or
"gluten content does not exceed x parts per million."Then we will see the
tens of millions of gluten-sensitive consumers placed in a much better
position to make more informed, healthier decisions for themselves.
Common Sources of Contamination
If you live in a household where some residents are eating gluten, a
shared toaster can be a source of difficulty. Sharing the same butter dish
can also result in sharing a certain amount of gluten, perhaps enough to
perpetuate sensitization.
10
Dangerous Grains
3. there are isolated areas of cancer treatment that actually do improve
the quality of life and longevity for a minority of cancer patients
Despite die consistent failure of a majority of cancer therapies, there
is often a quick dismissal of even mildly divergent perspectives, especially
when they involve diet. It seems that many, at least in the realm of cancer treatment, have few answers hut considerable disdain for the views of
others. However, the scientific evidence simply does not support such a
narrow view.
The avoidance of dietary intervention is confusing and disturbing.
Many of today's mainstream cancer treatments sometimes cause horrible
suffering to patients during the declining season of their lives, yet we
have repeatedly heard the foolish assertion that a giuten-free diet will diminish the quality of the cancer patient's life. Purveyors of such nonsense
should try following a gluten-free diet before uttering such thoughtless
remarks.
WHAT ARE THE LIMITS OF OUR
K N O W L E D G E OF CANCER?
Of course, if we had a full understanding of cancer, we would soon know
the cure. Sadly, there is neither a complete understanding of cancer nor a
reliable cure. For the most part, there are only contested theories and
very debatable treatments, with a few rays of sunshine in an otherwise
dismal scene.
There are at least two important ways in which our current knowledge of cancer is quite limited. We not only have an incomplete understanding of cancer—perhaps because of the narrow research focus dictated
by economics and politically correct medicine—but we also have some
mistaken ideas about the nature of the disease. It is the second limitation
that poses the greatest problem. We often cling to many mistaken notions
with an amazing tenacity. Perhaps desperation strengthens our grip, as
cancer deaths continue at an alarming rate.
The Cancer Connection
107
Historically, there are many examples of dearly held mistaken beliefs.
Childbed fever, an infection transmitted by medical personnel, was once
blamed on its victims. Pellagra, a deadly disease of nutritional deficiency,
was once considered an infectious plague. The history of science is riddled with examples of such mistaken beliefs, which slow and misdirect
research. To avoid this, until we can honestly claim significant cure rates,
we should remain open to additional information and alternative perspectives. It is the absence of openness that limits the massive health-care
and research industries concerned with understanding and treating cancer.
Many current cancer treatments are crude, cruel, costly, and often
deadly. Cancer research proceeds at a dead-slow pace. While we await the
very gradual expansion of knowledge about cancer, we must work with
the evidence we have.
LET'S LOOK AT WHAT W E DO K N O W
We already know that cancers are very rare or nonexistent in primitive
cultures consuming hunter-gatherer diets. We also know that where wheat
and its near relatives are cultivated, we see the gradual emergence of
cancer.
For instance, increased cancer risk among female farmers in Norway
maps a clear connection between exposure to wheat and cancer, although
the researchers reporting this connection blame the molds that grow on
wheat for these cancers. In the United States, a correlation between
wheat cultivation acreage and cancer deaths has been reported, although
this increase was attributed to pesticide use. Other studies have suggested
that whole-grain consumption will increase the risk of developing prostate
cancer. Although the researchers consistently blamed other features of
grain cultivation, there is a clear connection between the amount of grain
that is grown and rates of cancer. Despite the popular belief that grains
prevent colorectal cancer, some studies have shown that consumption of
refined flours actually increases the risk of colorectal cancer.
In a report of children following a gluten-free, dairy-free, low-residue
10
Dangerous Grains
diet following conventional cancer treatments, there were huge reductions in the rate of enteritis, a condition that often results from abdominal radiation and chemical therapies for cancers. In this study, the rate
dropped from 70 percent to zero. Not a single case of enteritis developed
among those patients who followed this diet! Enteritis, with its associated infections and malnutrition, is frequently the cause of death in such
cancer patients, so it is difficult to exaggerate the importance of this
study.
In cases where celiac disease has been identified at the same time as
cancer, there have been a few cases reported where a change in diet, in
addition to conventional treatments, resulted in full remission of the cancer. In one case, a gluten-free diet certainly led to the disappearance of
enlarged lymph glands that may have signaled lymphoma. Yet another
patient with celiac-associated lymphoma improved when the only therapy was a gluten-free diet in combination with nutritional supplements.
There have also been reports in the peer-reviewed literature of cancer
patients in the grips of apparently hopelessly fatal cancers who have experienced dramatic improvements and recoveries on a ketogenic diet.
This diet provides energy through fats, not carbohydrates. Although this
is a much stricter, more difficult diet to follow, it starves the cancer cells
of the glucose they need to reproduce. It is the relentless reproduction of
cancer cells and their displacement of healthy ones that is cancer's greatest threat. By slowing or halting this reproduction, the ketogenic diet allows the immune system a window of opportunity to battle these aberrant
cells. Because this diet excludes gluten and can be dairy free, avoidance of
opioids for pain management unleashes natural killer cells to attack the
malignant ones.
This diet, originated in the 1920s, has recently received considerable
public attention, as it can often control epileptic seizures when no known
drug is effective. Bart of the success of this diet in the treatment of such
cases of epilepsy and cancer may also lie in its total exclusion of gluten.
Among those with celiac disease, the gluten-free diet has been shown
to reduce the risk of developing cancer after about five years of strict di-
The Cancer Connection
10
etary compliance. This is a group that otherwise has quite a large risk of
developing any of a number of cancers, especially intestinal lymphomas.
This research, and a great deal of other evidence, points to the astounding possibility that our growing gluten gluttony is a major contributor to escalating cancer rates today. The evidence against gluten is certainly
mounting. However, we leave the final judgment of that issue to future,
more adventurous cancer research and to the reader.
H O W DOES GLUTEN INCREASE
THE RISK OF CANCER?
There are certain peptides, or protein fragments, found in gluten and in
casein, a protein found in milk, that look and act just like the narcotic
known as morphine. They are hidden in an inactive state within the
gluten and casein protein sequence, and are released by the digestive
processes in the stomach and by pancreatic secretions. Once freed from
the larger protein structure, they are highly resistant to enzyme digestion
in the intestine. There is quite a large body of evidence establishing that
these peptides found in gluten and dairy products may also be responsible
for many of the health hazards associated with gluten. Some researchers
have suggested that the opioids were the primary attraction for our ancestors who adopted agriculture. The physical, sensual comfort offered
by the exorphins encouraged them to relinquish their healthier, less demanding hunter-gatherer lifestyles. Exorphins may be the determining
feature of what we now call "comfort foods."
Gluten contains at leastfive distinct opioids—A4, A5, B4, B5, and C —
and they are found repeatedly in the structures of a single protein. Gluten
exorphin, A5, for instance, occurs at fifteen sites in a single glutenin protein. Although exorphins are less potent (0.5 mg of the most active of
these exorphins are reported as about equal to InM of morphine) and
variable in their strength, there can be little doubt that such a plentiful
supply has helped shape the Western diet.
1
Dangerous Grains
They are called "casomorphins," and are not as potent as those derived
from gluten.
Recall that hunter-gatherers were apparently immune to cancer. For
at leastfive hundred thousand years, these ancestors of ours, with rare exceptions, did not eat a diet that contained gluten. Dr. Reading's cancer patients benefited from a gluten-free diet while undergoing conventional
cancer treatments, and Dr. Donaldson's pediatric patients who were otherwise at grave risk of developing enteritis have also given us cause to
value a gluten-free diet in the context of cancer treatments.
MALABSORPTION
Among those who recognize the threat of cancer for those with celiac
disease, it is commonly understood and accepted that diet and the essential nutrients found in foods play a critical role in the cause of many cancers. We have known for half a century that celiac disease is characterized
by a malabsorbing, leaky gut. Celiac patients not only leak larger proteins,
such as exorphins, into their circulation, but also fail to absorb many essential nutrients. This is usually thought to result from the reductions of
absorptive surface area in the small intestine. However; this view fails to
explain the broad variations in type and extent of nutrient deficiencies
that are displayed by untreated celiac patients.
There are many reports of a wride range of such deficiencies, including
deficiencies in the minerals calcium, magnesium, selenium, manganese,
copper, iron, and zinc and deficiencies in vitamins C, D, A, E, K, and a
wide range of B vitamins. And herein lies a serious difficulty in recognizing celiac disease. Deficiency in each of the vitamins and minerals listed
above will produce a set of symptoms that can usually be distinguished
from each other. For each deficiency, there is often a range of possible
symptoms and sets of symptoms. Sometimes, the number of variations in
symptoms for one deficiency can be quite surprising. When compounded
by the interaction of several or many deficiencies, the range of signs and
symptoms can be enormous and quite confusing.
The Cancer Connection
INSULIN ABNORMALITIES
To further add to the confusion, exorphins have repeatedly been shown
to cause increased insulin production and release. Insulin is a hormone
that moves glucose into cells. This means that many of the calories that
celiacs absorb are likely to be stored as fat, rather than circulating in the
blood and being available for energy demands. It is therefore not surprising that obesity has been found to be more common than wasting, among
untreated celiac patients. Neither is it surprising that most untreated celiacs fall within the normal range for body mass, despite suffering from a
disease involving malabsorption. The most sinister part of the increased
insulin blood levels is that cancer cells need glucose for tumors to grow.
This may explain the higher incidence of cancer reported in adult-onset,
non-insulin dependent diabetes. The increased insulin production caused
by gluten-derived exorphins not only masks malabsorption but also helps
to feed tumors, accelerating their growth. The impact of exorphins on insulin production is likely another factor in the increased cancer rates
among untreated celiacs.
THE ROOT OF THE CONFUSION
This confusing array of nutritional factors, and the signs that point to
them, has some serious implications for diagnosing celiac patients. They
also have some serious implications for many cancer patients. For instance, investigation of cancer patients for gluten sensitivity might offer
new cause for hope. The evidence certainly suggests that a gluten-free
diet can be very helpful to many cancer patients, but without suspecting
and testing for gluten sensitivity, we will never know how many cancerprone individuals the diet might help.
In summary, gluten consumption, in isolated groups, has been shown
to increase the risk of cancer. Grain farming has also been shown to increase
the risk of some cancers among grain farmers. Similarly, a gluten-free diet
1
Dangerous Grains
has been shown to reduce the risk of cancer in some of these groups. A
gluten-free diet, sometimes in addition to elimination of other foods, has
also been shown to be beneficial to cancer patients, especially in conjunction with conventional therapies. For many reasons—from morphinelike substances hidden in the proteins of these foods, to the nutrient
deficiencies and abnormal intestinal permeability they cause, to the impact of exorphins on insulin production—-gluten is a food that cancer patients should be urged to exclude from their diets.
Gluten consumption increased in the United States and Canada
throughout the last century. Our increased consumption of processed
foods and the diet fads touting high grains/carbohydrates has combined
to encourage this steady increase. In parallel with the increased consumption of gluten grains, the rate of cancer deaths has risen from
2.5 percent in 1900 to nearly 30 percent, where it now rivals and will
soon surpass cardiovascular disease as the primary cause of death in the
United States, Given the evidence, a causative relationship between increased gluten consumption and cancer should be highly suspect.
The next several chapters combine to suggest why and how gluten
cereals have managed to turn our immune systems against our own
bodies—the system that is our primary defense mechanism against all
disease.
Gluten, Molecular Mimicry,
and Autoimmune Disease
S
ixty-five to 68 percent of celiac children and adults have circulating
antibodies that attack some of their own tissues—a characteristic of
autoimmune disease. However, only 6 percent of normal subjects were
found to have such autoantibodies. One group of researchers further
reported that more than 20 percent of celiac patients had evidence
of autoimmunity, including antithyroid and antipancreatic antibodies. A
large majority of the celiac patients with these an ti-self antibodies were not
following a gluten-free diet. One of the most startling lessons we learned
from our study of gluten sensitivity was that simply eliminating gluten
from one's diet can reduce the body's production of these antibodies.
Further, given the elevated gliadin antibodies among patients with
autoimmune diseases, in the absence of celiac disease, the evidence suggests that gluten sensitivity may be the most important factor that predisposes to autoimmune diseases. There are many autoimmune diseases
that are affected by gluten, but we have chosen to explore just a few ex-
Dangerous Grains
amples to demonstrate gluten's effect on the many forms of autoimmunity We first show the overlap between autoimmunity and celiac disease,
then a similar overlap with non-celiac gluten sensitivity. Finally, we report
on the impact that a gluten-free diet has on the patients with specific autoimmune diseases and celiac disease. A gluten-free diet is often just as
helpful to those non-celiacs who show only anti-gliadin antibodies and
suffer from the same autoimmune disease.
Autoimmune diseases where gluten sensitivity and celiac disease should
be ruled out include:
• Alopecia Areata {sudden head
Idiopathic thrombocytopenic
baldness confincd to limited
Microscopic colitis
areas or patches)
Multiple sclerosis
• Arthritis
Nephropathy (kidney disease]
• Autoimmune thyroid disease
Optic neuritis
• Biliary atresia
Oral cankers (aphthous ulcers)
• Biliary sclerosis
purpura
• Cirrhosis (of the liver)
Sarcoidosis
• Crohn's disease
Systemic lupus erythematosus
• Diabetes mellitus
'Irigeminal neuritis
• Fibromyalgia
Vasculitis
• Hypoparathyroidism
C O N N E C T I N G AUTOIMMUNITY
TO GLUTEN
The connection between autoimmune disease and gluten grains is supported by evidence that is clear and compelling. We have already established that gluten leaked into the bloodstream will injure a wide variety
of human tissues. Such damage is likely a factor that leads to autoimmune disease, but that is far from the whole story. The risk of the many
autoimmune disorders common in celiac disease increases with the length
Gluten, Molecular Mimicry, and Autoimmune Disease
ll9
of time in which a celiac consumes gluten. Gluten sensitivity is also very
common in patients with a variety of autoimmune diseases. Taken together, the evidence leaves little doubt that gluten is at least a factor in
many, perhaps most cases of autoimmune diseases.
MOLECULAR MIMICRY
The most reasonable explanation we have found for the connection between gluten and autoimmune disease lies in a dynamic called "molecular mimicry," especially as it applies to food allergy. Molecular mimicry is
driven by the fact that very different proteins are frequently made up of
similar structures. When proteins that make up our own tissues appear
similar to "invader" proteins, our immune systems will attack our own
tissues. When foreign proteins, or large fragments of protein, enter the
bloodstream, their presence is sensed by the immune system, which interprets them as non-self and potentially harmful. The immune system
then begins production of antibodies that are specifically tailored to identify and destroy these invaders. These antibodies react just as they would
to the foreign proteins of infectious agents such as bacteria and viruses.
At the same time, the immune system also produces memory cells, which
remember and recognize certain parts of the structure of this invader
protein, should it enter the blood again.
The specific part of the protein sensed by the antibody is a set of
amino acids. It is this set of amino acids, called an "epitope," to which the
antibody attaches itself. Like a combination lock, these groups have a
number of amino acids arranged in a specific order. The memory cells recognize the invader by the combination of amino acids in their protein
structure and signal for rapid production of many antibodies. They are
called antigen-specific antibodies because the immune system has constructed them to identify and attack only molecules with the identifying
sequence. This process is the basis of vaccination and acquired immunity.
12
Dangerous Grains
FOODS AND ABNORMAL
ANTIBODY PRODUCTION
When we eat a food such as gluten (most Westerners eat it several times
every day), we are likely to leak at least some incompletely digested, overly
large proteins into our bloodstream, even when we are in good health.
People prone to food allergy and gluten sensitivity are inclined to experience suppression of their digestive process, excessive leakiness of their
gut lining, and an abnormal influx of partly digested foods. Even if the
proteins are partly digested (due to the nature of the sulfide bonds holding gluten together, it is always poorly digested), the larger peptides from
gluten are likely to contain a sequence that will result in production of
specific memory cells.
If the small intestinal leakage continues on a day-to-day basis, antibody production will be kept at a very high level. This means that where
there is daily gluten consumption, suppression of digestion, and a leaky
gut, there will be excessive quantities of antibodies circulating throughout the body.
THE PROBLEM W I T H CIRCULATING
GLUTEN ANTIBODIES
Molecular mimicry, also called cross-reactivity, is thought to result in the
formation of specific antibodies formed to protect us from our external
environment—attacking internal molecules that display identical or very
similar amino acid sequences. If these sequences in food molecules are
duplicated in the structures that make up our own tissues, our antibodies
will attack these look-alikes: Our immune system turns against us. Autoimmune diseases such as insulin-dependent diabetes mellitus (IDDM),
thyroiditis, multiple sclerosis, and arthritis may be the end result. Alarmingly close similarities between gluten protein structure and the structure
of body tissues have been reported, sometimes in association with partic-
Gluten, Molecular Mimicry, and Autoimmune Disease
ular autoimmune diseases. We can only conclude that chronic leakage of
gluten proteins into the blood is a likely cause of autoimmune diseases.
GERMS AND MOLECULAR MIMICRY
Bacteria, viruses, and yeast probably do cause or contribute to at least
some cases of autoimmune disease, but the evidence suggests that the
majority of cases are, partly or wholly, the result of dietary proteins. Molecular mimicry requires chronic antibody production. So the trigger that
starts and continues to signal the immune system to produce antibodies
must be present on an ongoing basis. With a few exceptions, infectious
agents that penetrate the body's defenses are either neutralized or destroyed by the immune system in a relatively short time. Dietary proteins
such as gluten, on the other hand, are chronically present in the body, day
after day. If the immune system reacts by making antibodies against this
common food, then a gluten-containing diet may provide the necessary
trigger to start an autoimmune disease, and to keep it going.
Conditions Necessary to Activate
Gluten-Induced Molecular Mimicry
i
.1
1. regular consumption of gluten
2. a genetic predisposition, food allergy, or infectious assault that
causes an abnormally permeable intestine or "leaky gut"
3. chronic absorption of large, incompletely digested molecules
into the blood, whether proteins or partial proteins
4. antibody production that recognizes parts of dietary "non-self
protein structures
continued
Dangerous Grains
INSULIN-DEPENDENT DIABETES
MELLITUS (IDDM) AND GLUTEN
PLEASE N O T E :
After the complete autoimmune destruction of insulin-
producing islet cells, a gluten-free diet does not reverse or stabilize IDDM.
Gluten-induced neurological damage is also commonly irreversible.
l
While less than A of 1 percent of all Americans have insulin-dependent
diabetes mellitus (IDDM), as many as 10 percent of all celiacs develop
IDDM, and up to 8 percent of IDDM patients have or will develop celiac
disease. Many authorities are now emphatically recommending that all
IDDM patients be screened annually for celiac disease after the initial
IDDM diagnosis. There are 1 million IDDM patients in the United States
today, with approximately thirty thousand patients diagnosed each year.
Clearly, there is considerable overlap between celiac disease and IDDM.
It is well established that celiac disease is the direct result of gluten. Our
first clue that gluten may be a major cause of diabetes is found in the
overlap of the occurrence of celiac disease and IDDM.
A recent report indicates that IDDM is generally on the rise, especially in populations that previously enjoyed low rates of this disease. We
suspect that this reflects worldwide increases in consumption of the diabetogenic foods-—gluten, soy, and cow's milk. Further, Finland and Sardinia are reporting two of the highest rates of IDDM in the world. These
are two of the three areas with the highest rates of celiac disease.
GROUP
PREVALENCE OF C E L I A C DISEASE
Saliarawi Muslim adolescent! in Morocco
I in 18
Northern Sardinia
I in 70
Finland
I in 85
Gluten, Molecular Mimicry, and Autoimmune Disease
From animal studies, we now know that among rats that are genetically
susceptible to IDDM, feeding wheat gluten will cause 40 percent to
develop IDDM. Several other groups of rats with the same genetic inclination to develop IDDM were fed gluten-free diets, and only 10 to 15 percent of these groups developed IDDM. Further, the rate and severity of
diabetes could be manipulated by varying the amount of gluten in the
diet. Others have shown that delaying introduction of dietary gluten in
animal models delays or prevents diabetes. Most authorities in this area of
diabetes research conclude that gluten is a major factor in causing the development of IDDM in genetically predisposed animals.
This work, along with other research over the past decade, has some
serious implications for an emerging therapy for IDDM patients. For example, a series of medical advances have made it possible to transplant
insulin-producing cells into diabetic patients. There are three major difficulties in this dramatic medical advance. First, when full insulin production is achieved, it is only temporary and lasts for an unpredictable period
of time. The second problem is that these transplants usually result in
only partial insulin production. A third concern is that the same autoimmune insulin-producing cellular destruction may occur if these transplanted diabetic patients continue to eat a gluten- or soy-rich diabetogenic
diet. We believe that the patients receiving these islet cell transplants
would benefit from excluding gluten, soy, and dairy products from their
diet.
Multiple Sclerosis-Diabetes Connection
Some startling new research has revealed that the overlap between
multiple sclerosis (MS] and IDDM is so great that they may simply be
different manifestations of the same disease. We have long understood
that MS patients produce antibodies that attack their own myelin, the insulating sheath on nerve fibers. MS researchers are now reporting that
many MS antibodies will attack insulin-producing cells. Further, they also
report that antibodies from most IDDM patients will attack the myelin
sheath on nerves. We anxiously await confirmation of these results and
Dangerous Grains
suspect that it is yet another point of convergence between gluten and
these two autoimmune diseases.
Type 2, Non-Insulin-Dependent Diabetes
The current explosion of Type 2 diabetes among our young people
points to an indirect result of our culture's gluten gluttony. Loading the
diet with so much carbohydrate (dominated by cereal grains) leads to downregulation of cellular insulin receptors. This chronic carbohydrate consumption and, hence, elevated blood sugar, have to cause excessive insulin
production, along with a tendency to overproduce the pro-inflammatory,
pro-cancer, pro-allergy, pro-cardiovascular disease, metabolism inhibiting
prostaglandin E2 series.
Both celiac disease and diabetes are major contributors to the epidemic
of magnesium deficiency and chromium deficiency Up to 90 percent of
Americans and Canadians consume less than the minimal 50 micrograms
of chromium a day. It follows that celiacs eating a normal diet would be
profoundly chromium deficient. Chromium deficiency is associated with
1. hyperglycemia
2. hyperinsulinism/insulin-resistance
3. insulin-dependent diabetes (IDDM, Type 1)
4. adult-onset diabetes (NIDDM,Type 2)
5. gestational diabetes (diabetes of pregnancy]
6. corticosteroid-induced diabetes
7. excessive body fat/lowered lean body weight
8. elevated total cholesterol
9. elevated LDL cholesterol
10. elevated apolipoprotein B
11. lowered HDL cholesterol
12. lowered apolipoprotein A-l
13. atherosclerosis
14. syndrome X (central [abdominal] obesity, diabetes, elevated cholesterol, high blood pressure, elevated triglycerides, etc.)
Gluten, Molecular Mimicry, and Autoimmune Disease
15. alcohol abuse
16. excessive consumption of refined sugars and cereals
AUTOIMMUNE LIVER DISEASE
AND GLUTEN
Chronic liver disease of unknown cause is common in celiac patients, and
a gluten-free diet usually results in improvements in liver enzyme profiles
along with resolution of the liver disease. Some researchers recommend
testing for celiac disease in cases where there is no known reason for elevated liver enzymes, reporting that 9 percent of these patients have celiac
disease. Other reports indicate high levels of gliadin antibodies among patients with liver disease in the absence of celiac disease.
Many individuals suffering from a range of liver diseases, including
biliary cirrhosis and chronic active hepatitis, have elevated anti-gliadin
antibodies in their blood. As many as 11 to 20 percent of patients with
cirrhosis and chronic hepatitis, depending on the type of liver disease, are
gluten sensitive. Yet, it was only among the patients with autoimmune
hepatitis that there was an increase in celiac disease.
Because cases of liver disease occurring in conjunction with celiac disease usually show dramatic improvement or complete remission on a
gluten-free diet, the connection with gluten is difficult to deny. It also
suggests the potential value of excluding gluten even among those who
are non-celiac gluten sensitive. The common misguided assumption that
elevated gliadin antibodies are meaningless or coincidental without biopsyproven celiac disease is inappropriate, and we think this assumption is
harmful to the patient. Dismissal of such results denies the patient the
opportunity to benefit from further testing or a gluten-free diet.
Dangerous Grains
RHEUMATOID ARTHRITIS AND GLUTEN
Rheumatoid Arthritis Alleviated
by a Gluten-Free Diet
I
started developing rheumatoid arthritis in 1990, By 1994 I could
hardly walk in the mornings. My hip joints were extremely stiff.
I could only shuffle forward and could not pivot my right hip.
My family doctor said that I would need a hip replacement operation someday. It was then that I started doing research into
gluten sensitivity, really on behalf of my mother, who suffers from
Crohn's disease. When I was reading about Crohn's disease, I discovered that not only Crohn's but also many other ailments were
being researched in the United Kingdom and United States in relation to gluten. The more I read, the more I realized that all these
symptoms wrere in my family,
I visited a registered dietitian and posed the questions; "Could
I be 'allergic' to gluten? Will I get Crohn's disease like my mother?"
The dietitian suggested that I go on a gluten-free diet for two
weeks, then test myself with a lot of gluten over three or four days.
What I discovered then has changed my life forever! My sinusitis
was completely gone in five to six months. My chronic constipation, which I had suffered since childhood, went away. I now take
no medication whatsoever. When I realized that I had saved myself
a hip replacement operation, I decided to start a support group. I
decided that there were many people that a change in eating
habits would help. I now work very hard to bring this information
to as many people as I can. It really is a message that needs to be
taken to everyone.
Lucille C.
Gluten, Molecular Mimicry, and Autoimmune Disease
The studies in medical literature on rheumatoid arthritis (RA) and juvenile chronic arthritis reveal both a relationship between these diseases
and gluten and some shocking facts about how often celiac disease and
gluten sensitivity are likely to be overlooked in many cases of these joint
diseases. This literature is also somewhat of an expose of the devastating
potential of gluten grains. Children with hauntingly painful and horribly
disfigured joints often wait years to be tested for celiac disease. When
they finally are tested, they will often test positive. For them, relief follows the gluten-free diet, although their disfigured joints will likely serve
as permanent reminders of that pain.
Researchers are reporting the occurrence of celiac disease over five
times more frequently among people with rheumatoid arthritis. The prevalence ranged as high as 7.5 percent. That is an occurrence that should
grab anyone's attention. More remarkably, about half of the patients with
rheumatoid arthritis show clear signs of gluten sensitivity through elevated
serum levels of anti-gliadin antibodies. More specifically, a variety of antibody blood tests has revealed non-celiac gluten sensitivity in 34 percent
of juvenile chronic arthritis patients and in 47 percent of adult rheumatoid arthritics.
Although such elevated antibody levels were long considered to be
the result of increased intestinal permeability caused by non-steroidal
anti-inflammatory drug (NSAID) pain management, there is now solid
evidence to counter this view. One study compared anti-gliadin antibody
levels from RA patients early in their disease with those who have advanced disease. They found that anti-gliadin antibodies are elevated in
48 percent of the patients who have recently developed arthritis, while
only 25 percent of those with advanced disease show elevated gliadin
antibodies. They suggest that their results may point to a gluten factor
that begins this destructive inflammatory joint disease in these patients.
We agree.
Reports of arthritis, after the discovery of celiac disease, indicate that
the arthritis pain either improves or completely resolves on a gluten-free
diet. There is often little need for pain relief after a few months on the
diet. There are only a very few exceptions where the condition continues
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to progress, perhaps due to some mechanism that becomes independent
of gluten, making the condition chronic. One group investigated the impact of fasting followed by a gluten-free, vegetarian diet (not what we
would recommend) on a group of rheumatoid arthritis patients. They reported significant objective and subjective benefits.
The agonies imposed by arthritis require medications for pain management that risk significant, often debilitating, side effects, including kidney failure, bleeding ulcers, perforation of the intestine, acceleration of
joint destruction after ten years on medication, and early death. Yet many
arthritis patients are reported to suffer for two tofifteen years before they
are finally tested for celiac disease. A cursory viewing of the X rays of
these patients' joints is heart wrenching, and such delays seem needlessly
cruel.
It is difficult to imagine a rational argument against first ruling out
celiac disease and non-celiac gluten sensitivity, especially when they are
both found so frequently in many types of arthritis. Yet, individuals with
gluten-caused or aggravated rheumatoid arthritis may never be t o l d —
may never be given the option of the diet because non-celiac gluten sensitivity is too often dismissed as "nonspecific,"
We strongly urge the routine blood testing of all arthritis patients for
delayed-onset food allergy and gluten sensitivity, and, if allergic foods are
identified, strict exclusion of those foods should be prescribed.
Both Food and Infection May Contribute
to Rheumatoid Arthritis
rb further complicate the issue, one group of researchers has presented evidence revealing that a combination of dietary protein and bacteria contributes to the progression of rheumatoid arthritis. Diet-induced
intestinal permeability allows leakage of "friendly" bacteria from the intestine into the bloodstream, where it travels to, and becomes bound to,
joint tissues. The immune system attacks, damaging both the intestinal
bacteria and the joint tissues to Which these bacteria are bound.
Gluten, Molecular Mimicry, and Autoimmune Disease
CANCER CONVERGENCE W I T H OTHER
AILMENTS IN CELIAC DISEASE
People with autoimmune disease have increased risk of celiac disease,
as do intravenous drug users. Celiac patients also experience an increased
risk of cancer and autoimmune diseases. While these occurrences may
seem unrelated, these associations actually point to an important issue
when looking at cancer risk.
In autoimmunity and celiac disease there is increased intestinal permeability, allowing leakage of partly digested proteins into the blood,
many of which have repeatedly been shown to have opioid activity. Many
addicts, of course, inject opiates directly into the bloodstream or tissues
adjacent to blood vessels. These food-derived peptides and infected drugs
have an important feature in common: They signal natural killer cells in
our immune system to slow or stop their normal activities. Through this
process, called "downregulation," we lose the activity of the very cells that
are the body's first line of defense against disease and, in particular, malignancy. Due to this opioid activity, our immune system is inhibited from
identifying and destroying the body's tissue cells that have damaged or
fragile chromosomes, thus preventing them from becoming cancerous.
MODEL FOR THE DIETARY TREATMENT
OF AUTOIMMUNITY
The evidence presented here indicates that routine testing for celiac disease and gluten sensitivity should be conducted on all patients with
autoimmune disease. The evidence also suggests that treatment with a
gluten-free diet may offer dramatic improvements far beyond those offered by medications aimed at pain control or down-regulating the immune system. Dietary therapies, although more controversial, do not cause
the often unpleasant, and sometimes very dangerous, side effects associated with drugs, especially those used for pain management.
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A study on psoriasis (a very unpleasant autoimmune skin disease)
serves as a model for connecting gluten with autoimmunity. Several
anecdotal reports suggested that psoriasis might be more frequent in
celiac disease. But, when investigated, the connection was not supported.
Testing of a group of 302 patients with psoriasis revealed that 16 percent
showed at least one type of antibody against gliadin. Within this group,
two patients had celiac disease, or approaching 1 percent, which is reflective of the general population. However, these researchers then enrolled the non-celiac gluten-sensitive patients with psoriasis in a dietarystudy. Of the thirty patients wrho stayed with the strict gluten-free diet,
the entire group showed a significant decrease in the signs and symptoms
of psoriasis. When they returned to a regular diet, as part of the study,
more than half of these people experienced a resurgence of psoriatic symptoms. The report unequivocally recommends a gluten-free diet as a treatment for psoriasis patients wrho have anti-gliadin antibodies.
CONCLUSION
Celiac disease and non-celiac gluten sensitivity often underlie autoimmune disease. Gluten is the common thread that connects many forms
of autoimmunity, including the four types of autoimmunity that we have
used as examples to demonstrate this connection.
A majority of those with untreated celiac disease show at least some
indication of additional forms of autoimmunity Further, autoimmune
thyroid disease is overrepresented among those with celiac disease, and
celiac disease is overrepresented among those who have any form ol autoimmune thyroid disease. A similar overlap is seen in insulin-dependent
diabetes mellitus, autoimmune liVer disease, and rheumatoid arthritis.
Of at least equal importance is that non-celiac gluten sensitivity is
also overrepresented among those with these autoimmune diseases. Although the connections between celiac disease and autoimmunity are
well documented, the celiac patient must often be proactive and request
appropriate testing and follow-up.
Gluten, Molecular Mimicry, and Autoimmune Disease
Unfortunately, celiac disease and non-celiac gluten sensitivity are often differentiated, which may lead to less satisfactory' medical advice.
Positive test results showing gluten sensitivity may be dismissed on the
assumption that such results are nonspecific. Patients may not be encouraged to follow a strict gluten-free diet. More commonly, their immune reactions to gluten may never even be mentioned.
In autoimmune disease, we recommend testing for both celiac disease
and gluten sensitivity. When patients have positive antibody tests for
either, a gluten-free diet should be followed.
Osteoporosis
and Gluten
was diagnosed about thirteen years ago with celiac. I weighed
112 pounds, and 1 am six feet one inch tall. I was still walking/
working, but barely. I had stress fractures in my feet. My vision
had deteriorated to the point where I was getting a new prescription about every six months. I was having nosebleeds every day
along with headaches, abdominal cramps, leg cramps, muscle twitching, tingling in my fingers and toes, bone pain, etc. About three
days after going gluten free, I felt better, i had to get new prescriptions on my glasses about every six months due to vision improvement. My hair grew back. I gained about 60 pounds over
three years.
Jim B.
Osteoporosis and Gluten
135
If you have weak, porous bones, you might want to eliminate gluten
from your diet even if you do not mount an immune response to this
food. A significant portion of our society is plagued by this silent disability. The first painful hint of a problem is often a broken bone. There are
several ways that gluten can interfere with maintaining strong, healthy
bones. In this chapter, we explain how gluten can cause this crippling and
painful malady.
According to the National Osteoporosis Foundation, osteoporosis is a
major public health threat for more than 28 million Americans, 80 percent of whom are women. In the United States today, 8 million women
and 2 million men already have osteoporosis, and 18 million more have
low bone density, placing them at increased risk for osteoporosis; hip,
back, and wrist fractures; and premature death.
Approximately 250,000 Americans die annually from the complications associated with hip fractures. Co-author James Braly's father was
one such osteoporotic hip fracture victim.
Cases of bone degeneration are increasing at an epidemic rate. Much
of it is due to our aging population, of course, with women now living
well beyond eighty and men following closely behind. But that is only part
of the explanation. Current dietary recommendations are shortsighted and
out of date, reflecting a simplistic view of the many factors that contribute
to building and maintaining strong, healthy bones.
The source of much of this poor advice is the infamous USDA food
guide pyramid. Its proponents have failed to keep pace with current research. Despite exploding numbers of cases of osteoporosis and the welldocumented, negative impact of gluten consumption on bone density,
daily consumption of six to eleven servings of cereal is still recommended.
Such recommendations are akin to urging a drowning man to drink more
water. These recommendations are a clear denial of much of what we
now know about bones, how they grow, and what makes them strong.
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GLUTEN CAN ALSO CAUSE
OSTEOPOROSIS IN THE
NON-GLUTEN SENSITIVE
Phytate is the storage form of most phosphorus found in plants. It has a
strong attraction to a variety of minerals including calcium, magnesium,
iron, and zinc. Even for people who do not suffer from gluten sensitivity,
phytates are cause for concern. They are found in large quantities in the
outer layer of cereal grains. During digestion, especially in the stomach, phytates will combine with calcium and other minerals. The bonds that form in
these chemical combinations are resistant to the human digestive process,
so important minerals will be wasted when phytates are consumed. Therefore, by eating whole grains we decrease the availability of those dietary
minerals that help us grow and maintain strong, healthy bones.
GLUTEN, VITAMINS, AND BONE HEALTH
Further, grain consumption often displaces fruits and vegetables that are
good sources of some important vitamins needed to keep our bones healthy.
Vitamin C contributes to bone maintenance by aiding in the production
of collagen. Production of this connective tissue is needed not only for the
repair of bone breaks but also for the replacement of aging collagen that
is destroyed by osteoclasts in the normal turnover of bone tissues.
Vitamin K is deficient in the diets of many women, many celiacs, and
most people suffering from osteoporosis. At one time, vitamin K, an essential vitamin derived from food and the action of intestinal bacteria,
was thought to be involved solely with the clotting of blood. As it turns
out, vitamin K is needed in other key processes, including the production
of osteocalcin by osteoblasts. Osteocalcin is a bone protein important in
bone metabolism and bone formation. When excessive levels are found in
the blood, it is associated with bone disorders such as Paget's disease and
postmenopausal osteoporosis.
Osteoporosis and Gluten 137
The January 1999 issue of the American Journal of Clinical Nutrition
reported on more than seventy-two thousand women who were divided
on the basis of their consumption of vitamin K. Those who consumed the
most vitamin K were only 70 percent as likely to have broken a hip as
women in the group that took in the least amount of this important vitamin. More impressive was the observation of lettuce consumption. Women
who ate vitamin K-rich lettuce at least once a day were 45 percent less
likely to have a hip fracture than those who ate the same food once a
week or less. Consuming less than 109 micrograms of vitamin K resulted
in bone thinning, but more than 109 micrograms did not add any more
protection against hip fracture.
For women ages fifteen and older, federal guidelines recommend consuming 180 micrograms of vitamin K each day, probably an excessive
amount. On the other hand, the RDA for vitamin K is 65 micrograms for
women and 80 micrograms for men, which is probably too low.
The research findings clearly demonstrate that other nutrients besides
calcium are important for maintaining healthy bones. Instead of the current
narrow focus on calcium, women ought to be sure to eat a well-balanced
diet containing enough protein and vitamin K. In addition to broccoli,
lettuce, and other leafy vegetables, foods rich in vitamin K include pork,
liver, and vegetable oils.
Vitamin A deficiency, another problem that often arises from gluten
consumption, can cause stunted growth in children and can also impact
on adult bones. Because this vitamin coordinates both bone-building and
bone-destroying cells, a deficiency may cause a wide range of bone abnormalities. To ensure sufficient vitamin A in your diet, eat foods such as
fish, flax, and liver, which are rich in this important vitamin.
BONES ARE VERY MUCH ALIVE
Bones are living tissue. Calcium, magnesium, zinc, and other minerals are
deposited and removed on an ongoing basis. Connective tissues within
bones and supporting the bones are renewed regularly. This work is con-
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ducted by cells that are bone builders (osteoblasts] and cells that are bone
destroyers (osteoclasts]. Our bones are made up of about 25 percent water, 25 percent protein, and the rest are mineral salts, mostly calcium.
Collagen is the connective tissue that provides the flexible framework on
which these brittle mineral salts crystallize. In healthy bones, this combination results in strong, somewhat flexible bones. The minerals provide
rigidity, and the collagen provides flexibility while reinforcing the minerals, much like the principles that give reinforced concrete its strength.
WHAT IS OSTEOPOROSIS?
When our bones are broken by mild impact or by normal, day-to-day
stresses, they are not healthy. Weak bones usually have more and larger
spaces between the mineral crystals that weaken bones by making them
porous. By now, it will be no surprise for you to learn that gluten can
cause this terrible, debilitating condition. Contrary to the current, unfortunate dietary fad, dairy products may also be contributing to many cases
of osteoporosis.
Adult-diagnosed celiacs invariably suffer some degree of demineralization of their bones. The extent of this damage can be quite dramatic.
WHAT CAUSES OSTEOPOROSIS
IN CELIAC PATIENTS?
For a long time, it was assumed that widespread osteoporosis among celiacs was the result of malabsorption. While it makes sense that we would
be unable to absorb enough calcium, resulting in a deficiency, when researchers looked more closely at this issue they found that the evidence
doesn't support such a simplistic view. It seems that gluten has a greater
impact on calcium metabolism than on actual absorption because it increases how much calcium we waste after it is absorbed. A gluten-free
Osteoporosis and Gluten
139
diet often results in dramatic improvements to the mineral content of
celiac patients' bones, but this is largely due to increased retention of
calcium.
A related paradox of osteoporosis and celiac disease is that calcium supplementation does not help to remineralize celiac patients' bones as much
as magnesium supplementation. There is comparatively much less magnesium in our bones, so this information provides an important clue to
the fascinating puzzle of the impact that gluten can have on bone density.
Not only is magnesium important to the activation of bone-building
osteoblasts that deposit calcium and add collagen to our bones but is also
a factor that aids in repairing the parathyroid gland. This is a gland that
produces the hormones (PTH) that regulate most of the body's calcium
metabolism. These hormones signal the kidneys to recover calcium from
the urine, to elevate blood levels of calcium, and to activate vitamin D
(calcitrol), which signals the intestine to absorb calcium from the food
we eat. Clearly, adequate dietary calcium is of little value if we are not
getting enough magnesium for the parathyroid gland to function properly.
For these reasons, dairy products and calcium supplementation may
actually have a negative impact on the density of our bones, exactly the
opposite of what we were taught to expect. It also counters the simplistic advice to consume calcium supplements alone and/or dairy products
that are often offered to many individuals with declining bone density
Magnesium, calcium, zinc, boron, and vitamins D and K, all reported to
be deficient in many celiacs, are absorbed from the intestine by the same
mechanism, called "active transport." Loading the digestive tract with calcium alone overwhelming invites this part of our absorptive capacity
with a single mineral, albeit the most common one in the body. This
approach is shortsighted and, quite frankly, harmful. It risks causing a
deficiency of magnesium and other necessary minerals, which are less
abundant and frequently deficient in our diets. Magnesium and phosphorous deficiencies caused by excessive calcium intake may pose a much
greater risk of causing bone mineral loss. Further, the risk is largely independent of the traditional suspect in gluten-induced bone damage—
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malabsorption. The key issue is the balance of relative quantities in which
these minerals are available, either in our diets and/or the supplements
we consume.
Great care should be taken in recommending calcium supplementation, especially among those who already suffer from bone demineralization and among those at greatest risk of developing such problems. A
typical, healthy intestine only absorbs a small portion of the calcium that
is available from our food. At the same time, evidence suggests that excess calcium intake competes with magnesium absorption, further aggravating a poor magnesium status. Flooding our diet with more and more
calcium is a dangerously simplistic approach to this complex problem.
Many hospital emergency rooms are now using large therapeutic doses
of intravenous magnesium as one of the first-line therapies for cardiac
patients. Such magnesium treatments have been shown to reduce the
extent of damage to the heart muscles and tissues. More and more medical clinics and emergency rooms are also beginning to use IV magnesium
as a first-line therapy to abort migraine headaches and asthma attacks.
The effectiveness of these therapies also suggests a common condition of
chronic magnesium deficiency. We view this common deficiency as a predictable result of our culture's obsession with magnesium-depleting consumption of massive quantities of dairy products and cereal grains.
THE PARATHYROID GLAND
Recall that, in untreated celiac disease, the parathyroid gland releases an
excess of parathyroid hormone, the single most important hormone for
regulating calcium metabolism. This is associated with abnormally high
bone turnover and bone loss. We now have evidence that, at least in some
cases of celiac disease, endomysium antibodies (the same ones that are
sought in screening tests for celiac disease) will cross-react with parathyroid tissues, resulting in damage to this important gland and compromising its ability to effectively regulate our calcium metabolism. Thinning of
Osteoporosis and Gluten
141
the bone, increased bone fragility, and proneness to low-impact bone
fractures are the consequences.
The tragic underdiagnosis of celiac disease and gluten sensitivity certainly suggests the need for more frequent screening for these conditions
among those with reduced bone density. Such testing should be conducted as early as possible to allow early and extensive gains in mineral
deposition, resulting in strong, healthy bones prior to declining production of sex hormones and growth hormones later in life.
OSTEOMALACIA AND GLUTEN
Another bone-density ailment that can also be related to gluten consumption is osteomalacia. This is a condition where the bones are very
flexible and weak. There appears to be ample collagen, but calcium, phosphorus, and/or other necessary minerals for bone hardness are lacking.
The childhood equivalent of osteomalacia is rickets. Both are often the
result of deficiencies in vitamin D. Recall that it is the active form of vitamin D, calcitrol, that signals the intestine to absorb more calcium and
other minerals from our food.
In osteomalacia and its milder form, osteopenia, our bones bend and
become deformed due to a deficiency of absorbed minerals, and this condition can often be halted and reversed by simple vitamin D supplementation. Unfortunately, bone deformations usually are not corrected. Those
who get little exposure to unimpeded sunlight, perhaps due to their jobs,
age, or medical condition, are at risk. Those who live in temperate zones
of the world run a seasonal risk of developing this problem.
Impaired kidney function, where there is excessive calcium excretion,
can also result in rickets, osteomalacia, and osteopenia. There is clear
evidence that gluten contributes to at least some cases of impaired kidney
function.
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THE IMPACT OF AGING AND SEX
HORMONES O N BONE HEALTH
All of the above factors in building and maintaining dense, healthy bones
become increasingly important as we approach middle age. The sex hormones estrogen and testosterone stimulate the action of bone-building
osteoblasts. As women experience menopause and men approach their
sixties, production of these sex hormones is reduced. Bone building
therefore slows and begins to be outstripped by bone destruction. If we
have built up strong bones in our early years, if we continue with weightbearing exercise regularly, and if we are eating and absorbing adequate
quantities and an appropriate balance of all the necessary minerals, our
bones should continue to serve us throughout our old age. If we are gluten
sensitive or have celiac disease, even if religiously pursuing a gluten-free
diet, we may need to take aggressive action, supplementing magnesium
and ensuring adequate vitamin D intake or absorption.
If you have a personal history of osteoporosis or osteopenia, periodic
bone-density tests should be done to assure that your gluten-free diet and
supplementation program are working optimally for you.
BACK TO THE FUTURE
Gluten and dairy products are two of the most allergenic foods in our
food supply. As we have shown, calcium supplements as a primary or sole
nutrient intervention and consumption of gluten and dairy products can
actually threaten our absorption of other important minerals, compromise our bones and general health, and cause the very disease they are
purported to prevent.
As you have seen, there are many factors that affect bone health. Regular exercise, ample sunshine, a varied non-allergenic diet, and a variety
of vitamins are needed, along with several important minerals and hormones. All of these factors must work in a balanced, harmonious manner
Osteoporosis and Gluten
143
to build and maintain strong bones. Any change in this balance can lead
to sudden and measurable changes in a relatively short time. Substantial
improvements in bone density occur within one year of diagnosing celiac
disease and beginning a gluten-free diet. Excessive calcium supplementation, without a balance of other bone nutrients, may well contribute to
the very problem that it is aimed at helping.
A gluten-free, dairy-free diet that includes a wide range of meats, organ meat, fish, poultry, vegetables, and fruits, with moderate quantities
of non-gluten grains, is not only closer to the one we evolved to eat but
also one that will give us strong, healthy bones. Given the importance of
an optimally functioning parathyroid gland for bone health, the crossreaction between endomysium antibodies and the parathyroid gland also
suggests that there may be autoimmune factors contributing to the bone
damage caused by gluten.
Brain Disorders
and Gluten
odern gluten gluttony has even invaded the private recesses of our
minds. In this chapter we outline many of the psychiatric and neurological problems that can result from gluten sensitivity. The elimination
of dietary gluten might soon replace many more expensive and ponderously slow conventional psychiatric treatments,
A BRIEF HISTORY OF GLUTEN'S EFFECTS
O N MENTAL HEALTH
As many celiacs will attest, periods of fasting will provide at least a partial
recovery from the symptoms of celiac disease, including relieving chronic
depression and sleeping problems, and cause a strong overall sense of psychological well-being. There are many cases throughout history demonstrating the impact of diet on mental health. Starvation was used in
Brain Disorders and Gluten
145
ancient Greece to treat insanity. More tellingly, during World War II, the
prevalence of schizophrenia dropped precipitously among European populations where there were grain shortages. If schizophrenia is, in large part,
the result of gluten-derived opioids, the ancient strategy of fasting might
well be quite an effective short-term strategy.
A very active research group at the Royal Hallamshire Hospital in
Sheffield, involving the departments of neurology, gastroenterology, and
histopathology, has demonstrated that gluten is a factor in a wide range
of neurological conditions. More than half of the fifty-three patients with
neurological conditions of unknown causes showed antibodies against
gliadin. Of these thirty patients, nine had celiac disease. The other twentyone of these patients were obviously gluten sensitive.
THE W I D E RANGE OF THE
NEUROLOGICAL EFFECTS OF GLUTEN
What must it be like to live your life never knowing if, just at a critical or
dangerous moment, you will have a seizure? Imagine the sense of uncertainty and vulnerability. Or what must it be like to experience the daily
corrosion of what was once a good memory? What must it feel like to
lose the ability to walk? Or the ability to talk? Worse yet, what must it
feel like to experience an internal world that is partly made of visual and
auditory hallucinations but is also partly the external objective world that
others share? These are only a few of the many powerfully negative
neurological consequences of eating gluten.
Many common brain diseases are known to be associated with high
rates of both celiac disease and non-celiac gluten sensitivity. These include
ataxia, peripheral neuropathies, or other such "chronic neurological conditions of unknown cause" (note: most chronic neurological conditions
are of unknown cause). This also includes senility, another extremely
common brain disorder that often appears to be related to gluten sensitivity. In senility, however, one has to catch and treat the mental deterioration early in order to prevent its progression. Unfortunately, continued
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deterioration despite a gluten-free diet is common in late-stage senility.
For this reason, we will focus on prevention, through early detection and
treatment of gluten sensitivity.
While the disorders of degeneration, blood circulation, and seizures
can alter behavior, emotions, and learning, there are many more conditions that are affected by gluten. Psychological depression, neurotransmitter deficiencies, autism, and hyperactivity disorders can also be brought
on by gluten sensitivity. These other brain diseases are associated with important changes to the brain, but, unlike epilepsy and senility, there is
no visible structural brain damage. The evidence points to the action of
gluteomorphin, a morphinelike substance that is derived from dietary
gluten, as an important cause of these conditions.
You may want to examine your genetic heritage and determine whether
you might be at risk. But the first step is to understand how gluten and
its derivatives affect the brain, then to have a careful look at the specific
behavioral, psychiatric, and neurological conditions that have been connected to gluten.
ANTI-GLUTEN ANTIBODIES THAT
ATTACK THE BRAIN
We know that hallucinations, epilepsy, and disordered blood supply
within the brain are easily explained by the actions of gluten or its derivatives. There is mounting evidence that these abnormalities may be the
result of the interaction between our immune systems, gluten, and selftissues. In blood taken from untreated celiac patients, researchers found
antibodies that attack blood vessel walls in the human brain. Only three
individuals in the control group showed gluten sensitivity, but none of
this latter group showed antibodies as did the above untreated celiac
patients.
Relatedly, when cats are fed gluten, they develop structural abnormalities in the brain. Celiac patients experience a wide range of neuro-
Brain Disorders and Gluten
147
logical ailments that have also been shown to involve changes to the
brain's structure.
Taken together, this evidence suggests that the antibodies of celiac patients sometimes enter the brain, where they can cause irreversible damage in some cases of epilepsy, chronic schizophrenia, and progressive
neurological conditions. In other cases, such as newly diagnosed or newly
relapsed schizophrenia, epilepsy, and disordered blood distribution in the
brain, there may be a rapid improvement on a gluten-free diet.
ERGOTISM
Even the molds that grow on gluten grains have proven to pose a serious
neurological and mental-health threat. Ergot is a fungus that will grow on
any of the gluten-containing grains when they become damp for an extended period, but it is most frequently found on rye. Ergot poisoning, or
ergotism, was known in the late Middle Ages as St. Anthony's Fire. People suffering from St. Anthony's Fire were sometimes accused of witchcraft because of the seizures and hallucinations caused by ergot. This
reaction to ergot is not surprising, considering that this mold is the source
from which the hallucinogenic drug LSD is refined.
Although ergotism occasionally afflicts domestic livestock, resulting
in neurological symptoms, and sometimes lameness and death, modern
grain-processing techniques usually provide good protection against it.
Grains used for human consumption are now treated with much more
care. Today, people are rarely afflicted with ergotism, and then it is usually due to overuse of certain drugs intentionally derived from rye molds
grown in the laboratory. Such drugs are sometimes used to treat the excessive expansion of blood vessels in the brain that usually underlies migraine headaches. In fact, rye-mold derived ergot is such an effective
constrictor of blood vessels that ergotism often results in lameness, followed by gangrenous tissue decay due to the poor circulation to the
affected limb.
Dangerous Grains
Peptides derived from gluten grains have since been implicated in
schizophrenia, epileptic seizures, and vascular illnesses and are sometimes
found to occur among patients who also have celiac disease. Like ergot,
these peptides have recently been shown to affect blood flow within the
brain, attention deficit hyperactivity disorder, and autism. Taken together,
this information clearly suggests the connection between bioactive peptides derived from grains and the many disorders that also manifest gluten antibodies.
MOOD, BEHAVIOR, PSYCHOLOGY,
AND GLUTEN
When looking at the kinds of brain and neurological injuries and ailments
commonly found in celiac disease and gluten-sensitive patients, one finds
extremely interesting and important patterns. Mood is often reflected in
behavior. Disturbances of mood have long been recognized in celiac patients. From the very earliest reports, statements such as the following
have characterized celiac children:
The temper of the child seems variable, most frequently he is extremely irritable, fretful, capricious, or peevish. Nothing seems to
please him, and altogether he is quite unlike himself.
This is a sentiment that has been repeated frequently in literature and
continues to be mentioned by researchers. One report indicates that 63
percent of celiac children present with aggressive, bullying, angry, or irritable behavior.
Depression has been claimed as the most common symptom of celiac
disease. Some researchers argue for routine blood testing for celiac disease
on the basis of behavioral disturbance or depression alone. Whether we
look at depression, anxiety, or behavior problems, such psychiatric symptoms are often eliminated by the simple removal of gluten from the diet.
Even among those with silent or asymptomatic celiac disease, a gluten-
Brain Disorders and Gluten
149
free diet often improves psychological well-being. In fact, some researchers
are recommending that celiac disease be recognized as a bio-psycho-social
disorder. Other researchers have warned that symptoms that appear to be
caused by psychological factors, such as recurring complaints of stomachaches and irritability after the birth of a younger sibling, may be the result of unrecognized celiac disease.
Attention Deficit Disorder
(with or without Hyperactivity)
Disorders of mood and mind are also common in people who experience difficulty in maintaining their attention, but the most prominent
feature of attention deficit disorder is the inability to maintain focus and
attention where there is not a strong emotional motive. Whether the
afflicted individual is lethargically disinterested in her or his surroundings
or is hyperactive and unable to settle into a task, the attention-challenged
individual in question may well be suffering from gluten sensitivity.
About 70 percent of children with untreated celiac disease show exactly the same abnormalities in brain-wave patterns as those who have
been diagnosed with attention deficit disorder. Another recent study, the
first of its kind, reported that food allergens, including wheat, could reproducibly cause abnormal brain waves. The most remarkable part of this
research is that it shows that after a year of excluding gluten from the
diet, all of these abnormalities disappear. For these children, diet not only
treats their celiac disease but also their brains and ADD.
Celiac children also show dramatic improvements in mood after a
short time on the diet. Since celiac disease afflicts about 1 percent of the
population, and gluten sensitivity afflicts many more people, and since
there are identical abnormalities in the brain-wave patterns of celiac children and ADHD children, it seems likely that there is a significant overlap between these groups. Given the evidence for overlap with gluten
sensitivity, we think it is very likely that many people afflicted with attention deficits would benefit from a gluten-free, food allergen-free diet.
ISO Dangerous Grains
Learning Problems and Gluten Sensitivity
The learning problems associated with celiac disease and immune reactions to milk proteins are related but separate issues. One study looked
for dyslexia, a learning disorder marked by an inability to recognize and
comprehend written words, in 291 fourth-grade children. Of the fifteen
children who were determined to have dyslexia, two were subsequently
diagnosed with celiac disease, and one had antibodies against milk protein . If these findings reflect the rates of celiac disease and/or milk protein
intolerance among dyslexic children, then diet may offer a powerful remedy for dyslexia. These children were placed on a gluten- and dairy-free
diet, but follow-up data are not yet available.
Other learning disabilities, including both short-term auditory memory
and slow visual processing speed, are much more common in celiac disease
than in the general population, especially among male patients. We can
only speculate about what such a diet might offer to those dyslexics who
do not show immune reactions to these foods, but the evidence appears
to warrant blood tests and a personal experiment. Dyslexia is a condition
that has lifelong career implications and can have a powerful impact on
self-esteem.
Alcoholism and Gluten
Inspired by the work of Theron Randolph, M.D,, Joan MatthewsLarson, author of Seven Weeks to Sobriety, has reported significant food allergies in 73 of the 100 alcoholics she studied. She also reported that Herbert
Karolus, M.D., found that most of the 422 alcoholics he studied were allergic to wheat or rye. Alcohol consumption causes and worsens abnormal
intestinal permeability and is thought by many to be bodi the cause and
effect of food allergies. Food-allergic and gluten-sensitive individuals often
report more frequent and severe allergic reactions to foods in conjunction
with alcohol consumption. Because of the genetic component in alcoholism, we suspect that the predisposition to alcoholism also predisposes to
an abnormally permeable intestine and proneness to food sensitization.
Brain Disorders and Gluten
151
Schizophrenia
Medical science took yet another leap forward when Dr. F. Dohan, a
Philadelphia researcher and psychiatrist, learned that schizophrenia is
frequently found in people with celiac disease, and celiac disease is frequently found in people with schizophrenia. He further found that in
cultures where gluten-containing grains are rarely eaten, schizophrenia is
rare or nonexistent. His dogged pursuit of this connection is the wellspring of a whole new understanding of diet-induced mental illness, and
his work serves as a model for investigating other dietary ailments.
Unfortunately, schizophrenics are rarely tested for gluten sensitivity. A
more recent report provides a startling example of this connection. A
thirty-three-year-old man who was previously diagnosed with schizophrenia showed reduced blood flow to a frontal lobe of his brain. This
is common in schizophrenia as well as in brain-sensitive food-allergic
patients. This young man later developed some of the classic signs and
symptoms of celiac disease, so he was tested. After he began a gluten-free
diet, not only did his celiac symptoms disappear but also his symptoms
of schizophrenia. Further, and perhaps more important, the pattern of
blood flow in his brain also normalized.
This case, of course, is powerful support for Dohan's pioneering work
in this area, but it is also vastly more than that. This one case connects
compromised blood flow or blood vessel constriction in the context of
schizophrenia and celiac disease. It also establishes gluten as the cause of
this constriction by demonstrating that the constriction resolves on a
gluten-free diet, and the patient recovers from both ailments.
This finding has implications for a range of ailments from strokes,
to seizures, to autism, to aneurysms, to severe headaches. Migrainelike
headaches are overrepresented in people with celiac disease and gluten
sensitivity. Symptoms improve on a gluten-free diet, and celiac disease is
overrepresented among those who chronically experience severe headaches.
Conventionally, ergotamine is the prescribed medication for the treatment of migraine headaches. Ergotamine causes constriction of blood
vessels, thereby reducing the pain caused by vessel expansion in the brain
2
Dangerous Grains
of a migraineur. Eliminating allergic foods, including gluten, also can result in the elimination or lessening of migraine pain. Our position is that
it is no accident that ergotamine is refined from a fungus that grows on
gluten-rich rye and other grains.
Similarly, the hallucinogenic drug LSD is also derived from molds that
grow on gluten grains. The hallucinations experienced in ergotamine poisoning may result from similar peptides gaining access to the brain. Some
celiac patients undergoing a gluten challenge also experience hallucinations. Although there is not enough evidence to assert a connection, there
is certainly enough to raise our suspicions about gluten as the common,
underlying element in these conditions.
Taken together with gluten-derived exorphins, the impact of grains on
schizophrenia seems evident and predictable. As a biochemical ailment,
schizophrenia serves as an excellent reminder that psychiatric illness is
just that—an illness. And many cases involve exorphins, peptides that
cause blood vessel expansion and contraction, changes in neurotransmitter balance, and hallucinations.
EPILEPSY
Our case against gluten is particularly strong in the areas of gluteninduced epilepsy and disorders of blood vessels in the brain. Severe epileptic seizures, particularly those associated with calcium deposits in the
brain; migraine headaches; and/or hyperactivity, often respond very well
to a strict gluten-free diet. These improvements sometimes reduce or
eliminate the need for antiseizure medications, even in cases where seizures had previously been poorly responsive to drug therapies.
In most cases of epilepsy, seizures can be lessened or eliminated with
drugs, but about 20 to 30 percent of cases do not respond well to drugs.
For some of these seizure victims, a diagnosis of celiac disease can have
some very positive results.
Published reports of food allergy-induced seizures go all the way back
to 1914. Although there were a few reports of the causative relationship
Brain Disorders and Gluten
153
between celiac disease and epilepsy prior to the late 1980s, the connection has received increasing attention over the last fifteen years or so.
Celiac-associated epilepsy has been reported to occur in connection with
migraine headaches, hyperactivity, calcium deposits in the brain, and in
cases of blood vessel abnormalities in the brain. Celiac disease is now well
recognized as a factor in most cases of epilepsy where calcium deposits
are found in certain regions of the brain.
For some time, such connections were thought to be more than coincidence, but the issue was never investigated. Finally, in 1998, in a study
where the prevailing rate of celiac disease was established at 1 in 244
pregnant women, celiac disease was found in 4 of 177 epileptic patients.
That translates to a rate of 1 in 44 people with various forms of epilepsy
who also have celiac disease. Judging from that research, celiac disease
appears six times more frequently among those suffering from epilepsy.
The occurrence of celiac disease is probably even greater among those
with epilepsy associated with calcium deposits in the brain, although that
question awaits further research.
Perhaps the most encouraging element of this connection between
gluten and seizures is that some people with epilepsy find that their
seizures stop after they begin the diet. Others report that their seizures
are less frequent and easier to control with drugs when following a
gluten-free diet. The evidence suggests that many individuals living with
epilepsy would benefit from such a diet, regardless of their test results
for gluten sensitivity. Unpredictable seizures and unpleasant side effects
from antiseizure medications both seem a greater hardship than switching to a gluten-free diet.
AUTISM
Autism is another increasingly prevalent brain disorder where a strict
gluten-free and dairy-free diet shows surprising, at times startling, improvements. The improvements were marked by better eye contact, less
hyperactivity, enhanced verbal and cognitive skills, and greater sociability,
Dangerous Grains
Symptoms of Autism Reversed
on a Gluten-Free Diet
y son first developed bowel problems as a small child subsequent to his immunizations. He was also constipated alternating with diarrhea. He descended into autism. He was unable to
make controlled movements, a condition called apraxia. He was almost nonverbal. The speech therapist had to use sign language to
work with him. This was at four years old. He had almost no
speech and few appropriate play skills. He could spend up to eight
hours a day switching lights off and on.
The school psychologist said that he belonged in a county-run
preschool class. I observed the class and saw kids curled up in corners. They were low functioning with no apparent speech capability. The professionals said that with luck, by elementary school, my
son would be in a special "autistic" class, possibly mainstreamed in
one or two nonacademic areas. His future seemed very bleak.
I did some research on the Internet, then had my son tested for
food allergies. He showed antibodies to dairy and gluten. I began
removing gluten from his diet when he was between four and five
years old. He has been strictly gluten free with only a few accidents. The results have been amazing. He went from being totally
in his own world to being an engaged child. The cloud lifted.
Now-, at nine, he is in a regular classroom, performing at grade
level. He just won the school spelling bee, is on a baseball team,
and is a competitive Irish dancer.
1 am very glad I was able to access the Internet and read the
works of Ron Hoggan, Ray Audette, and others.
Mary H.
Brain Disorders and Gluten
155
in a substantial majority of cases, but the diet does not seem to completely cure the disorder.
Autistic children show strong evidence of delayed-onset IgG mediated food allergy, including recurrent middle-ear infections, epilepsy (onethird of autistics will suffer from seizures by adolescence), red ears,
powerful food cravings, leaky gut, pronounced digestive problems, sleep
disorders, hyperactivity, abnormal blood flow to certain areas of the brain,
and many other conditions associated with gluten sensitivity.
Autism is another example of a condition where there is often no detectable celiac disease, but where gluten sensitivity plays a key role. Why,
then, do many autistic children improve on a gluten-free, dairy-free diet?
We think it has more to do with a complex interaction between digestive
enzymes and intestinal permeability. Absorption of partly digested gluten
and other foods, in combination with an abnormally permeable intestine,
is an important part of this incomplete picture.
The successful but highly controversial use of an injectable form of
synthetic secretin, a gut hormone, in the treatment of autistic children is
another direction from which there is support for the role of a gluten-free
diet. Research shows that secretin receptors are found not only in the intestinal tract, but the heart and brain tissues as well. Amazingly, the brain
secretin appears to influence cognition, emotions, and behavior. Dietary
gluten in an untreated celiac patient is a powerful inhibitor of secretin release, reducing blood levels of secretin by 90 percent. Eliminate gluten
from the diet, and blood secretin levels return to near normal. A majority
of autistic children experience improvements in cognition, behavior, emotions, verbal communication, and eye contact.
In another controversial study, Andrew Wakefield and his research
team demonstrated that there is an increase in intestinal permeability,
which may result from prior immunization in some autistic children. Such
increased intestinal permeability suggests a path into the bloodstream for
opioid and other peptides from partly digested gluten and dairy proteins.
A study by K. L. Reichelt and his colleagues reported abnormal quantities of urinary polypeptides in autistic children, which improved dramati-
Dangerous Grains
cally, along with similarly dramatic symptom improvement, on a glutenfree, dairy-free diet.
For some time now, measurements of urinary peptides have revealed
that autistic, schizophrenic, and depressed patients excrete large quantities of peptides that can function as neurotransmitters. Such increases
may be either a direct or an indirect result of leakage of exorphins into
the bloodstream. This important clue to the cause of at least some cases
of these psychiatric illnesses may indicate that these psychoactive peptides are small enough to be ignored by the immune system but function
as potent neurotransmitters.
Autism-Gluten Connection
There is further evidence supporting the connection between gluten
and autism. Paul Shattock, a plant biochemist and lecturer at the University of Sunderland, began collecting data and evaluating research when
his son was diagnosed with autism in 1974. When he heard speculation
that autism may be the result of peptide poisoning, he began investigating the possibility that gluten and dairy were at the root of his son's condition. Similarly, Kalle Reichelt, a researcher at the Pediatric Research
Institute in Oslo, Norway, also became interested in the possibility that
peptides from gluten and dairy products contribute to autism in his patients. By 1990, Reichelt and Shattock had learned through their own investigations that 90 percent of the autistic patients they studied have
abnormally high levels of urinary peptides. The evidence suggests that
these peptides are from dairy products and gluten cereals.
This research, in conjunction with earlier work by Dohan, has established a connection between gluten consumption and several types of
mental illnesses, behavioral problems, and learning disabilities. However,
broader recognition of these discoveries is slow.
Concerned parents and others may want to act more quickly on this
information, as the appropriate diet is very safe and nutritious. Other than
the inconvenience of implementing the diet while ensuring optimal nutrition, there is no known downside to this therapy. Those who currently
Brain Disorders and Gluten
157
struggle with these conditions will be unlikely to benefit from this information if they await its general acceptance before changing their diet.
MULTIPLE SCLEROSIS (MS) AND GLUTEN
A degenerative disease of the central nervous system, MS is another
condition where improvements have repeatedly been reported after beginning a gluten-free diet. It is a condition that is characterized by damage resulting from the immune system's attack on the fatty coating on
nerves, called myelin, which serve as insulation for nerves. This insulation
allows the speedy passage of impulses along nerves. Without myelin, the
neurological dysfunction of MS soon follows, resulting in symptoms that
include chronic fatigue, loss of balance, clumsiness, reduced vision, bouts
of localized paralysis, bladder problems, muscle spasticity, weakness, numbness, depression, and intellectual changes. The famous British playwright
Roger MacDougall reported his own amazing recovery from a terribly
disabling form of MS. Although he experienced a remission, not a cure,
his improvement was nothing short of miraculous.
How did he do it? As a result of his reading and research, Professor
MacDougall reasoned that his condition was the result of a chemical imbalance and that his best hope was to eat a diet that probably shaped human evolution. He cleverly decided to follow a diet that closely paralleled
that of a prehistoric hunter-gatherer—one that excluded dairy and gluten.
MacDougall not only experienced a dramatic recovery but also went on
to write about his recovery and the means by which he achieved it in a
pamphlet published by Regenics, Inc., a vitamin company with offices in
the United Kingdom and United States.
Four years after his own diagnosis of multiple sclerosis, Scottish biochemist Norman Matheson, Ph.D., was inspired by MacDougall. Although
not as debilitated as MacDougall, Dr. Matheson experienced a speedy recovery as a result of a gluten-free diet. His report appeared in the October 5, 1974, issue of Lancet.
Although in his declining years Matheson questioned the utility of the
Dangerous Grains
Gluten-Causing Symptoms of MS
A
few years ago I found myself faced with what doctors suspected were a growing number of symptoms of multiple
sclerosis. I was experiencing extreme muscular, neurological, cognitive, and gait abnormalities.
With some encouragement from a friend and support from
family, I found my way to a Paleolithic diet. 1 tried it with a "nothing to lose" attitude. To my surprise, my symptoms began to fade
within the first few weeks.
Through trial and error, I've found it was processed foods that
had caused my health to be greatly compromised. Foods containing gluten cause the most severe reaction. Within a few hours of
an accidental ingestion, symptoms return. I then have a minimum
recovery period of a week before symptoms subside.
It wasn't what E needed to add to my diet, but rather what
I needed to delete (all processed foods] that was key to my
recovery.
Patti V.
diet, his astuteness and alert demeanor would he considered a blessing to
any elderly MS patient fortunate enough to live so long with the disease.
Still, we do realize that the evidence only supports dietary intervention in some MS patients. We also acknowledge that other factors may
play key roles in MS, including excessive oxidative stress from vitamin E,
glutathione, C o Q 1 0 deficiencies, and increased intestinal permeability. To
our knowledge, only one group has investigated intestinal permeability in
MS. They found that 25 percent oi the MS patients they investigated had
increased intestinal permeability. This increase may simply allow gluten
proteins to leak into the bloodstream. As we established in an earlier
Brain Disorders and Gluten
chapter, these proteins have been shown to injure a variety of human tissues. However, it is a likely possibility that partial or whole proteins from
gluten are leaked into the bloodstream and that they trigger an inappropriate attack by the immune system on the MS patient's myelin.
CONCLUSION
There are many brain and nerve disorders that can be impacted by eating
gluten, A great deal of research is needed to clarify the role that gluten
plays in these ailments. Much of it will have to wait for at least another
decade as knowledge of the health hazards of gluten becomes more widespread. In the meantime, readers of this book who are challenged by
gluten-induced brain and nerve diseases will have to find their own way
through the labyrinth of confusion surrounding these conditions, hopefully linking with other like-minded individuals who recognize the importance of diet in these conditions.
Dangerous Grains
IRRITABLE BOWEL SYNDROME (IBS)
First, let's look at irritable bowel syndrome, or IBS. Although people with
IBS may look normal and healthy, they suffer from chronic stomach cramps
or pain, diarrhea alternating with constipation and bloating, and many
psychological symptoms. It is the most common bowel disease in the industrial world, afflicting about 22 percent of the Western population,
conservatively estimated at about 85 million people. Dr. Joseph Murray
of the Mayo Clinic in Rochester, Minnesota, has presented data showing
that about half of those with untreated celiac disease fit the diagnostic
criteria for IBS, known as the ROME criteria. That means that in the absence of blood tests and/or intestinal biopsy, we can expect that many
people with celiac disease currently have a diagnosis of IBS.
These findings are reflected in other research. One group of researchers
found that 12 percent of the group of IBS patients they studied actually
had celiac disease when they were tested for it. Another group reported
that 20 percent of their IBS patients suffer from celiac disease. Think that
one over for a moment. These studies indicate that anywhere from 10.2
to 17 million people are likely to have undetected celiac disease. Such reports indicate that a very significant minority of the people suffering
from IBS would greatly benefit from a gluten-free diet.
Non-celiac gluten sensitivity is much more common than celiac disease. Therefore, many, perhaps most, patients with IBS who do not have
biopsy-provable celiac disease may still be gluten sensitive and would
benefit from a gluten-free diet. Like all deductions, our conclusion is only
a reasonable probability until it is tested. However, the clues and evidence are quite persuasive.
Although they may share common symptoms, we make a clear distinction between celiac disease and IBS. Often poorly understood, IBS is
also poorly defined and is usually diagnosed through the exclusion of
other diseases. IBS frequently responds poorly to conventional medical
therapies. On the other hand, there is a clear, well-established diagnostic
protocol and very effective treatment for celiac disease.
B
Dises
and Gluten
163
A gluten-free diet has often been found to alleviate some or all of the
symptoms of IBS. For example, it has been reported that up to 70 percent
of all IBS patients improve with food exclusion. The majority improve
with the individual elimination of wheat, and many others benefit from
exclusion of oats and rye. We can only surmise that exclusion of all gluten
grains would be a valuable therapy for most of these patients.
Percentage of 122 IBS Patients Intolerant to Glutens and Other Foods
CEREALS
FRUIT
wheat 60% citrus 24%
corn 44%
VEGETABLES
DAIRY
MEAT
MISCELLANEOUS
onions 22%
cow's milk 44%
beef 16%
coffee 33%
cheese 39%
pork 14%
eggs 26%
apples 12% potatoes 20%
oats 34%
cabbage 19%
butter 25%
chicken 13% tea 25%
rye 30%
sprouts 18%
yogurt 24%
lamb 11%
barley 24%
peas 17%
rice 15%
carrots 15%
chocolate 22%
nuts 22%
Hunter,J.O., et al."Dietary studies." In Topics in gastroenterology 12, ed. R R. Gibson and D. P.Jewell
(Oxford: Blackwell Scientific, 1985), pp. 305-13.
Why, you might ask, in the face of such evidence, would the potential
therapeutic value of a gluten-free diet be ignored? The answer is simple:
Celiac disease is defined by biopsy-proven damage to the lining. Such
damage is not found in about 80 percent of people with IBS, so a glutenfree diet is not yet considered an appropriate therapy for most cases of
IBS. A majority of 85 million IBS sufferers are condemned to a life of discomfort as a result of this narrow, outdated definition of gluten sensitivity. We recommend IgG and IgA anti-gliadin and EMA or tTG antibody
screening of all patients with IBS. Positive test results should lead to a
prescription of a gluten-free diet.
Dangerous Grains
INTESTINAL INFECTIONS, FOOD
ALLERGY, AND GLUTEN SENSITIVITY
Intestinal infection is another range of ailments where we recommend
antibody testing and a trial of a gluten-free diet. Gluten sensitivity is often a contributing factor in chronic diarrhea, even where infection is the
primary problem. It also makes sense to consider antibody testing since
those with untreated celiac disease are also at greater risk of contracting
infectious diseases.
For patients with chronic diarrhea that is poorly responsive to conventional therapies, it makes perfect sense to consider IgG ELISA delayed
food allergy, IgG and IgA anti-gliadin, and EMA or tTG celiac screening
tests.
CROHN'S DISEASE
Crohn's disease is somewhat different from celiac disease, although both
conditions share many symptoms and features. Crohn's disease is an inflammation of the full thickness of the bowel wall and may impact on
any part of the GI tract, from mouth to anus. The inflammatory injuries
in celiac disease, on the other hand, are restricted to the thin mucosal lining of the digestive tract and do not usually penetrate all layers of the
bowel wall. In Crohn's disease, however, patients develop openings in
the bowel wall, called fistulas, that actually allow the bowel contents to
take shortcuts between different parts of the small intestine. This results
in parts of the bowel where there is little or no movement of the contents. It doesn't take much of an imagination to appreciate how infectious and painful the areas that are isolated by fistulas can become.
Gluten-induced injury to the bowel wall is the primary, defining characteristic of celiac disease. But these injuries do not usually penetrate all
layers of the bowel wall. These distinctions become less clear with increased
attention to detail, but the general principle does differentiate the two
B
Dises
and Gluten 165
diseases. Does that mean that Crohn's patients would not benefit from a
gluten-free diet? The evidence suggests otherwise.
Crohn's patients have very high levels of antibodies against gliadin
proteins, indicating a leaky gut, an immune response, and sensitivity to
gluten. Yet, due to a failure to recognize non-celiac gluten sensitivity, conventional medical wisdom ignores positive blood tests and gluten's contribution to the pain suffered by these people. Crohn's patients may hear
advice suggesting that they avoid foods that bother them, but that is very
different than encouraging patients to follow a strict gluten-free diet for
several months or a lifetime. Silent celiac disease and delayed reaction to
food allergens can result in most people being unaware of which foods
are problematic. Many Crohn's patients may not know that they have quite
elevated levels of gliadin antibodies and therefore should avoid gluten.
Due to the difficulty in self-diagnosing food sensitivities, testing for
IgG and IgA anti-gliadin antibodies and for IgG delayed-type food sensitivities is probably the best approach to determining which foods should
be eliminated from a Crohn's patient's diet. Another alternative is to recommend that Crohn's patients keep a symptom and food diary to monitor any changes. Although much less accurate than blood testing, these
tools may prove helpful to some. Testing for the presence of antibodies
to foods or food components is by far the preferable alternative in this
situation.
ENTERITIS, FOOD ALLERGY,
AND GLUTEN SENSITIVITY
We have already discussed the benefits of a gluten-free, dairy-free diet for
those who develop inflammation of the small intestines, called enteritis,
as a result of cancer treatments. We suspect that similar benefits might accrue to some patients who suffer from bacterial and viral enteritis.
Regardless of the cause of bowel disease, we recommend a glutenfree, dairy-free diet in addition to other restorative therapies.
Dangerous Grains
SWOLLEN LYMPH GLANDS
AND GLUTEN
On physical examination some celiac patients appear to have developed
a malignant mass in their small intestine. A more discriminating investigation sometimes reveals that excessively swollen lymph nodes are the
problem. The swelling recedes on a gluten-free diet.
MICROSCOPIC AND
ULCERATIVE COLITIS
There is considerable genetic overlap between celiac disease and an inflammation of the colon, called microscopic colitis, and patients often reflect this association in their symptoms. If you suffer from colitis and it is
not getting any better, you may also have to deal with the complication
of celiac disease. Celiacs are similarly at high risk of developing microscopic colitis.
In addition to the symptoms, there are frequently elevated levels of IgG
and/or IgA gliadin antibodies in colitis patients. This strongly suggests
that gluten is a contributing factor in the signs and symptoms of colitis.
TAKING A POSITION O N GUT DISEASE
Given the evidence, we argue that treatment of any medical condition
connected with a leaky or malabsorbing gut ought to automatically include a food allergy-gluten-sensitivity workup, possibly leading to a recommendation of a gluten-free/food allergy-free diet. Beyond intestinal
diseases, conditions associated with a leaky or flat gut include a variety of
liver diseases, pancreatic diseases, and several eating disorders. Of course,
we make the same recommendation for autoimmune diseases, along with
Bowel Diseases and Gluten
/67
a host of other chronic conditions where the laboratory evidence points
directly to gluten as a factor in the disease process.
Do not misunderstand. It is far from clear whether gluten actually
causes the underlying disease, but it is very clear that exclusion of gluten
is likely to provide some degree of relief from many bowel symptoms. By
excluding gluten, many patients may be able to stop the escalating cycle
of increased intestinal permeability, leakage of gluten into the blood-
Gut Symptoms that Can Be Alleviated
by a Gluten-Free Diet
1
1
l. abdominal pain
2. chronic diarrhea of unknown cause
3. steatorhea (excessive fat in stools)
4. recurrent aphthous ulcers (multiple, painful canker sores)
5. nausea and vomiting
6. bloating, abdominal distention
7. flatulence
8. GI bleeding (often X-ray negative)
9. angular stomatitis
10. glossitis, macroglossia (enlarged, inflamed tongue)
11. gastric and duodenal ulcers (in patients unresponsive to conventional antibiotic therapies for Helicobacter pylori)
12. abnormal intestinal permeability (leaky gut)
13. pancreatic insufficiency
14. gut hormone inhibition (secretin and cholecystokinin, e.g.)
15. dyspepsia, esophageal reflux (5 percent of all such patients
have gluten-induced loss of small intestinal lining = duodenal
villous atrophy)
168 Dangerous Grains
stream, increased antibody production, increased tissue damage, increased
intestinal permeability, and increased need for symptom-chasing prescription medications.
Not surprisingly, all of the above symptoms are also common in celiac
disease. The point is simple. We are not genetically well equipped to consume these grains.
11
W h e r e to from Here? Research,
Theories, and Treatments
M
any of the theories related to gluten sensitivity and celiac disease
are still in their infancy, early adolescence at best. This is in large
part the result of the popular belief, perpetuated with the very best of intentions by cereal manufacturers, dietitians, and the USDA food pyramid, that gluten cereals are very healthy, wholesome foods for the masses.
If it is true that the slow advancement in gluten research is the result of
the scarcity of research funding, it is doubly true that many health professionals are not taking time to keep up with the mountain of published
research in this area.
In spite of an inevitable resistance to new ideas, research into the
health hazards of gluten cereals is becoming a dominant force. This very
good news can only lead to promising discoveries that will improve patient care as well as point the direction for future research.
On the other hand, as in any area of innovation, there are also mistaken beliefs that persist or even gain support. The notion that "celiac dis-
Dangerous Grains
ease is rare" is a classic example of this. Mistaken ideas risk poorer patient
care and increase human suffering.
Nevertheless, the current state of gluten research is overwhelmingly
positive, favoring rapid progress and improved patient care. Indeed, these
are good times.
Celiac disease, as a subset of gluten sensitivity, has received the most
research attention. Because there is a great deal more information about
celiac disease than other expressions of gluten sensitivity, it provides the
best window through which to examine most areas of gluten sensitivity
and, hence, the best starting point for discussing variations in gluten
sensitivity.
PROGRESS IS NOT SIMPLE OR EASY
At least on the surface, expansion of human knowledge in a given field
appears to be a linear progression moving from one advancement to the
next, ever increasing and broadening our understanding. However, a closer
look reveals that the growth of knowledge has never been that simple or
easy. Advances in gluten-sensitivity research are always punctuated by interminable delays and innocent errors stacked on top of lingering misconceptions.
If we expect to see the same clear, straightforward progress in gluten
research that accompanies more developedfields, such as surgery or trauma
care, we will be disappointed.
Nevertheless, new advancements and possibilities are happening right
now. Let's take a closer look.
FUTURE GLUTEN RESEARCH
Several areas of gluten research show great promise. For the last four
decades or so, the overriding belief has been that only gliadins in the gluten
protein, the peptides that cause villous atrophy, are harmful. Therefore,
Where to from Here? Research, Theories, and Treatments 171
the other peptides that make up gluten, such as the glutenins, are interesting, perhaps, but basically harmless. Current research is beginning to
refute this notion.
Glutenin
Van de Wal and colleagues have identified a glutenin peptide that activates T-lymphocyte immune cells in the small intestine in much the
same way as gliadin, suggesting that glutenin may also be involved in
the disease process. In addition, glutenin seems to cross-react with elastin,
the principal component of elastic tissues, suggesting that glutenin may
play a role in autoimmune diseases of the skin. Other studies indicate
that glutenin peptides are toxic to cells. Even worse news for those glutensensitive people who turn to rice as a dietary refuge, glutenin antibodies
appear to cross-react with rice, perhaps placing rice off-limits to many
glutenin-sensitive people.
Clearly, gliadin is not the only toxic component of gluten, and blood
tests that exclusively identify antibodies sensitized to gliadin appear to be
inadequate for identifying everyone who is gluten sensitive. Innovative
laboratories are currently developing a new IgG and IgA anti-glutenin
immunoassay to compliment the anti-gliadin test, which should be available sometime in 2002. We would encourage research into sensitivity to
the other gluten peptides, such as globulin and albumin.
Another approach would involve exposing blood drawn from treated
celiacs to similarly purified gluten. The absence of an immune reaction
would certainly support the notion that only the identified peptides are
harmful. We are skeptical. We suspect that we still have a great deal to
learn in this area and that there are many harmful proteins to be found in
gluten grains. Only further research will tell.
Issues that Should Shape New Research Designs
When a celiac patient is consuming a gluten-free diet, a gluten challenge often involves very large quantities of gluten over a fairly lengthy
Dangerous Grains
period, sometimes years, before the intestinal biopsy will reveal the anticipated gluten-induced damage. Clearly, the intestinal biopsy is not a
highly sensitive procedure that will always detect small quantities of
gluten in the diet. Yet, this is the test that usually serves as the basis for
the rationale used to justify the unfortunate practice of recommending
consumption of mait-flavored breakfast cereals and a general disregard
for small quantities of gluten in the diet. Negative endomysium antibody
tests are also used to justify the recommendation of these foods to celiac
patients. As we have established previously, these tests are least sensitive
to cases where the intestinal damage is less severe. The use of these tests
to support these recommendations is illogical.
Such recommendations may lead hospital staff to serve such foods to
celiac patients in the belief that it does no harm. Dietitians and gastroenterologists sometimes use the same faulty reasoning to recommend such
foods to celiac patients. We suspect that these recommendations are
rooted in the perspective that the gluten-free diet is unpleasant and that
this more liberal approach is considered more humane.
PROBLEMS W I T H CURRENT
RESEARCH METHODS
We also need to develop some new methods for conducting this research.
Placebo Effect
Because our minds can sometimes play tricks on us, researchers have
had to develop ways of telling whether a particular drug or therapy caused
subjects to experience improvements in whatever condition was being
studied or whether the subjects were reporting changes because of the
psychological impact of the research program.
W h e r e to from Here? Research, Theories, and Treatments
173
Double-Blind Crossover
The research method that has gained the widest acceptance is called
the double-blind crossover design. This approach does not allow either
the subjects or those administering the drug to know whether individual
subjects are receiving the placebo or the active drug. If the research requires that subjects be observed or tested, those performing the observations or conducting the tests must also be unaware of the grouping of
research subjects and the treatment they have been given. The researchers
and subjects are both said to be "blind."
The crossover part of the design requires that subjects experience
some exposure to both the placebo and the drug. For part of the experiment, a given subject will receive the placebo. For another segment of the
experiment, the same subject will receive the drug. There is often a washout period when neither the drug nor the placebo is taken. This is done
to ensure that the drug has been eliminated from the subject's system.
Responses during each period are recorded and then tabulated. The placebo
effect, where subjects report anticipated changes, can be reported along
with fairly accurate indications of the drug's effectiveness.
New Designs Needed for Dietary Interventions
Such approaches as the double-blind, crossover design are not well
suited to investigating dietary interventions. This is true for several reasons. It is difficult to mask the taste and texture of foods. The presence or
absence of gluten is very difficult to mask. Dohan et al. answered this
problem by placing all the inmates on a locked psychiatric ward on a
gluten-free, dairy-free diet. Both groups were also given a daily beverage.
One contained gluten, while the other did not. Unfortunately, this required that many of the hospital personnel be aware of which beverage
contained the gluten, so the design was not double-blind.
Further, most dietary intervention research cannot reasonably include
the incarceration of their human subjects in a locked facility.
There are some reports of research where containment on a locked
Dangerous
Grains
ward was already in place, but this feature was undermined by the practice of allowing visitors to bring food to patients during the experiment.
This work clearly shows some of the difficulty with dietary research.
Because of the general perception of the harmlessness of foods derived from gluten and dairy products, it is also difficult to control for outside contamination by staff members. Without appropriate support, the
generosity of staff and visitors threatens the integrity of dietary research,
even on a locked ward. When the aid of these individuals is enlisted, the
research design may be compromised if we adhere to the design that was
developed for testing drug interventions.
Another problem with the use of a double-blind, crossover approach
is that the impact of dietary substances is often delayed. This can result in
delayed improvements that show up during the placebo phase and failure to improve during the intervention. It is confounding results such as
these that undermine dietary research yet are the predictable result of
using research methods that were designed for, and are well suited to,
pharmaceutical research. Appropriate experimental designs for dietary
interventions are needed.
Symptom Chasing or Treating the Cause
Another factor in this mix is that advances in drug research continue
to provide increasingly sophisticated chemical tools for masking symptoms and manipulating body chemistry rather than pursuing underlying
causes of symptoms. Considerable expenditure of talent, time, and money
for symptom chasing invariably reduces available resources for the search
for underlying causes.
N E W PERSPECTIVES AND
PARADIGM SHIFTS
Many encouraging perspectives and exciting areas of research have
moved to the forefront among prominent researchers. As these new per-
W h e r e to from Here? Research, Theories, and Treatments
spectives are studied, new ways of thinking about and understanding celiac
disease and gluten sensitivity will develop.
Gluten and Viruses
One avenue of research is driven by the notion that celiac disease not
only needs the genetic predisposition but also requires the exposure to
particular viruses before it can develop. Antibodies against adenovirus 12,
for instance, are found much more commonly among those with celiac
disease. Gluten-induced illnesses, such as insulin-dependent diabetes, may
also be a case in point, where infectious agents have started the disease
process by causing a leaky gut and, hence, contamination of the bloodstream with food proteins and peptides.
Gluten and Germs
The germ theory, first postulated more than 150 years ago, suggested
that disease is caused by invisible atomies, which we now call microbes.
This theory, coupled with advances in surgical intervention, has driven
most medical research during the last century. These advances, along with
improved sanitation, a more abundant food supply, and an infrastructure
that permits rapid treatment of traumatic injuries, have all combined to
extend longevity. These are venerable achievements. However, the paradigm that was shaped by these theories and advances has also slowed and
misdirected research related to cancer, osteoporosis, autoimmunity, some
types of brain disease, celiac disease, and many types of bowel disease.
In other words, the current way of thinking is not only shaped by the
germ theory, it appears inconsistent with many of the imperatives of dietary diseases such as gluten sensitivity and celiac disease. For example,
despite compelling research to the contrary, whole-gluten cereals are still
touted as a healthy food by many medical doctors, most certified dietitians, and many health-food stores. This, of course, is changing, but much
too slowly. The unfortunate truth is that, at a time when literally tens of
thousands of published studies are indicating the medicinal value of diet
176
Dangerous
Grains
and nutrition, inadequate dietary instruction is being offered to physicians
and dietitians. Both groups continue to be swayed by outdated perspectives,, allopathic prejudices, NIH pronouncements, and the Department
of Agriculture's promotional literature, especially the infamous food
pyramid.
Reversal and Prevention of Autoimmune
Disease on a Gluten-Free Diet?
Studies involving lab animals genetically prone to insulin-dependent
diabetes [IDDM] when eating diabetogenic foods such as gluten cereals
have shown that, in advance ol the clinical expression of IDDM, there is
insulin cell inflammation and elevation of blood levels of anti-gluten IgG
or IgA antibodies, indicating a slow but inexorable progression toward
the clinical disease. With the elimination of the gluten cereals that are
provoking an immune response, the progression toward clinical IDDM
abates. This indicates that, with early detection and dietary change, IDDM
can be prevented and possibly avoided indefinitely Human studies involving siblings of diagnosed diabetic children are currently under way to
test this extraordinarily provocative hypothesis.
Similarly, a recent study involving patients with celiac disease and
autoimmune thyroid disease indicates that early detection of gluten sensitivity and gluten elimination not only causes anti-gliadin antibodies to
disappear, but thyroid-specific autoantibodies as well. This may not only
help to reverse autoimmune thyroid disease but also prevent the development of other gluten-associated autoimmune diseases.
Glutamine for Villous Atrophy and a Leaky Gut
L-glutamine, the most abundant amino acid in the blood, brain, and
skeletal muscle, is a tasteless, nontoxic, conditionally essential amino acid
that appears to be showing promise in the treatment of celiac disease. Research demonstrates that glutamine is the primary fuel for the lining of
the small intestine and immune system.
W h e r e to from Here? Research, Theories, and Treatments
177
When given in therapeutic doses (9-20 grams a day in divided doses),
it also releases growth hormone and increases the production of a powerful, detoxifying, antioxidant enzyme called glutathione peroxidase. Glutamine also seems to protect the intestinal lining from the destructive
action of alcohol, NSAIDS, and aspirin. It has been reported that glutamine is now the most popular anti-ulcer medication in Asia because it
heals and helps prevent peptic ulcers. In a recent study in Japan, 92 percent of ulcer patients given 1,600 milligrams of glutamine a day showed
complete healing of duodenal and peptic ulcers in four weeks. It is also
currently being administered intravenously to patients receiving major
abdominal and bone marrow surgery, therapy for third-degree burns, and
chemotherapy or radiation therapy for cancer.
From our perspective, the single most promising benefit of glutamine
is that, when removed from the diet, it may prevent and reverse villous
atrophy, a leaky gut, and the malabsorption of nutrients so commonly
seen in celiac disease and Crohn's disease.
We would conjecture that glutamine's primary value will not be to
substitute a gluten-free diet, but to help accelerate healing when initially
going off gluten and to lessen intestinal inflammation when gluten is inadvertently or intentionally reintroduced back into the diet.
There are many such murky issues in the infant field of immune reactions to grain proteins. Each issue warrants appropriate research, which
will translate into health benefits for many
Population Screening
Another new perspective, beginning with a general recognition that
celiac disease is a common but badly underestimated condition, has led
to recommendations that screening for celiac disease be performed in all
six-year-old children, regardless if symptomatic, in entire school districts
in Italy.
Italy is at the forefront of research in the area of population screening.
Italian researchers are now conducting AGA blood testing on all beginning students of entire school districts. Those who show IgG and/or IgA
178
Dangerous
Grains
anti-gliadin antibodies are then tested for the presence of endomysium
antibodies. Where parents give their permission, if the EMA comes back
positive, an endoscopy is conducted to look for the characteristic intestinal damage of celiac disease.
The first stage of this research first revealed that celiac disease was not
rare, even in a country that is relatively close to the Fertile Crescent and
where gluten forms a large part oi many traditional foods. The startling
rates found in Italy were the first step toward recognizing that populations further removed from the Fertile Crescent would demonstrate even
higher rates of celiac disease.
We highly recommend the same screening program for Canada and
the United States-—but with one caveat: Italian researchers are currently
focused on finding, diagnosing, and treating only celiac disease. While we
have great admiration for the exciting work they are doing in identifying those with celiac disease, we would respectfully recommend a glutenfree diet to all children who have non-celiac gluten sensitivity.
Such population screening and recommendations will predictably
result in improved health and longevity for all of the gluten-sensitive individuals who are identified by this work and follow the appropriate
treatment.
We look forward to the day when gluten-sensitivity testing will become routine. The time is rapidly approaching when you will be able to
determine your own gluten and food-allergy status in the privacy of your
own home with a simple self-administered, results-while-you-wait fingerstick. One or two drops of blood from your fingertip and within thirty
minutes you will have accurate information regarding your sensitivity to
gluten, gliadin, glutenin, wheat, and oats, along with common food allergens such as milk, soy, yeast, and eggs.
England-based York Nutritional Laboratories is currently researching
and developing this innovative technology and hopes to make it commercially available to health consumers in Britain, Canada, and the United
States sometime in 2002.
W h e r e to from Here? Research, Theories, and Treatments
179
Screening for Additional Food Allergies
Frequently, a celiac patient, although improved on a gluten-free diet,
will still experience chronic symptoms and illness. Recent clinical research
suggests that additional delayed-onset food allergies coexist with celiac
disease. When these allergens are eliminated from the diet, the residual
symptoms disappear.
Yet, currently, such food allergies are rarely sought. Again, this reflects
a perspective that is slowly surrendering to the growing body of evidence
in support of food-allergy testing and health benefits that derive from it.
But there is a long way to go. Desensitization therapies are still offered, steroids are still considered a reasonable alternative to the glutenfree diet, and dapsone continues to be offered as an alternative to the
gluten-free lifestyle. These perspectives, although waning, have some dangerous and deadly implications.
Understanding the Benefits
of a Gluten-Free Diet
We have often heard about how unpalatable the gluten-free diet is.
But we hear it from people who have never followed the diet. We suspect
this says more about the speaker than about the gluten-free experience.
Our own experiences argue the contrary prospective. We find the diet not
only healthful but also enjoyable and fulfilling. The faulty assumption
that excluding gluten is tantamount to deprivation, causing suffering, is
foolish and limited. It may also reflect the addictive impact that this food
can have on some individuals. More emphasis on educating the glutensensitive individual about the wide variety of palatable, tasty, gluten-free
alternatives and integration of knowledge from the new medical specialty
of addictionology are imperative.
New developments in screening and diagnostic tests should result in
improved rates of diagnosis and improved treatments. Many of us will
benefit from such advances.
180
Dangerous
Grains
Expanding Alternatives
Hopefully, advances in research may also occur in the area of farming
and food production. At a time when more gluten is viewed as superior
and highly desirable, pioneering work is currently aimed at developing a
genetic strain of wheat that is free of the gluten proteins identified as
harmful to celiacs. (Not surprisingly, genetically modified milk cows that
can produce casein-free milk are also under research development.) Only
time, effort, and money will tell whether or not the bakers and wheatloving consumers will embrace these new hybrids.
Some grains such as rice, amaranth, and quinoa are relatively hypoallergenic, so cutting-edge farmers, anticipating the trend, are slowly
converting to non-gluten cereal grain production. As always, the health
consumers, voting with their dollars, will persuade the farmers, General
Mills and Post breakfast cereal companies, and the Department of Agriculture to accelerate this encouraging trend. We also anticipate that advancing gluten research will encourage farmers and manufacturers to
produce and develop more gluten-free alternatives and hope that many
of these changes will result in the cultivation and marketing of foodstuffs
that are more consistent with our genetic heritage.
STAYING IN TOUCH
Much is happening in gluten research and clinical nutrition. Promising new
studies and ideas abound. Some of the ideas in this book will be replaced
by new insights as our understanding in this area expands. We would sincerely like to share with you these new findings and concepts as they appear, along with our interpretation and spin. You can stay in touch through
our web sites www.cerealkillers.com (Braly) and www.dangerousgrains.com
(Hoggan).
Common Signs and Symptoms
of Celiac Disease
Alopecia
Delayed puberty
Anemias, especially iron and folic acid
Dental enamel defects
Anorexia
Depression
Autism
Down syndrome
Autoimmune arthritis
Early menopause
Autoimmune connective tissue diseases
Febrile seizures
Autoimmune thyroiditis
Gallbladder dysfunction
Cerebellar ataxia
Gallstones
Cerebral and cerebellar atrophy
Idiopathic thrombocytopenic
Cerebral calcifications
purpura
Chromosome aberrations
IgA deficiency
Chronic fatigue
IgA nephropath infertility
Chronic liver disease
Insulin-dependentdiabetes
Colitis
Constipation
mellitus
Intestinal cancers
182
Appendix
A
Kidney stones
Osteomalacia
Linear IgA dermatosis
Osteoporosis
Low calcium
Pancreatic insufficiency
Low iron
Pica
Low magnesium
Pulmonary bleeding
Low vitamin A
Retarded motor development
Low vitamin D
Rickets
Low vitamin K
Sacroileitis
Low zinc
Schizophrenia
Mild ataxia
Short stature
Monoarthritis
Single generalized seizures
Muscular hypotonia
Spontaneous, low-impact
Neurological disorders
fractures
Obesity
Systemic lupus erythematosus
Obstructive pulmonary disease
White-matter brain lesions
APPENDIX B
Hidden Sources of Gluten
SAFE SOURCES AND INGREDIENTS IN FLOUR
Caveat: Always double-check for risk of contamination.
Acacia gum
Buckwheat
Flax
Alfalfa
Canola oil
Fruit
Algae
Carob flour
Gelatin
Almond
Cassava
Guar gum
Amaranth
Cellulose
Herbs
Arabic gum
Cellulose gum
Maize
Arrowroot
Chickpea
Maltodextrin
Artichokes
Corn
Methyl cellulose
Bean, adzuki
Corn flour
Millet
Bean, hyacinth
Cornmeal
Milo
Bean, lentil
Cornstarch
Nuts
Bean, mung
Corn syrup
Pea flour
Bean romano (chickpea)
Flaked rice
Peas
184
Appendix
Potatoes
Sesame seed
Tapioca
Potato flour
Sorghum
Tapioca flour
Psyllium
Sorghum flour
Teff flour
Quinoa
Soy
Waxy maize
Rape
Soybean
Whey
Rice
Spices
Wild rice
Rice flour
Sunflower seed
Xanthan gum
Seaweed
Sweet chestnut flour
Yam flour
UNSAFE SOURCES OF F L O U R — M A Y CONTAIN GLUTEN
Abyssinian hard
Edible starch
Semolina
Einkorn wheat
Semolina triticum
Baking powder
Farina graham
Shoyu
Barley grass
Germ
Small spelt
Barley hordeum
Graham flour
Soba noodles
Granary flour
Soy sauce
Barley malt
Groats
Spelt
Beer
Gum base
Sprouted wheat or barley
Bleached flour
Hard wheat
Stock cubes
Blue cheese
Kamut
Strong flour
Bran
Malt
Suet in packets
Bread flour
Matzo semolina
Tabbouleh
Brewer's yeast
Miso
Teriyaki sauce
Brown flour
Mononoccum
Triticale
Bulgar
Mustard powder
Triticum aestivum
Bulgar wheat
Oats
Triticum durum
Cereal binding
Oat straw
Wheat nuts
Chilton
Pearl barley
Wheat triticum
Couscous
Rice malt
Wheat germ oil
Dextrins
Rye
Wheat grass
Durum wheat triticum
Seitan
Wheat starch
wheat
vulgare
Adapted from http://www.celiac.com
Hidden Sources of Gluten
I8S
ACRONYMS THAT MIGHT SPELL "HIDDEN" GLUTEN
Fu—dried wheat gluten
HPP—hydrolyzed plant protein
HVP—hydrolyzed vegetable protein
MSG—monosodium glutamate
TPP—textured plant protein
TVP—textured vegetable protein
APPENDIX C
Autoimmune Diseases Frequently
Found in Celiac Disease
Alopecia areata
Idiopathic thrombocytopenic purpura
Arthritis
Microscopic colitis
Atresia
Multiple sclerosis
Autoimmune thyroid disease
Nephropathy (kidney disease)
Biliary sclerosis
Optic neuritis
Cirrhosis
Oral cankers
Crohn's disease
Sarcoidosis
Diabetes mejlitus
Systemic lupus erythematosus
Fibromyalgia
Trigeminal neuritis
Hypoparathyroidism
Vasculitis
APPENDIX D
Comprehensive List
of Gluten-Associated
Medical Conditions
1. Abdominal distension/bloating
2. Abortions recurrent (15 percent of conceptions in patients with celiac
disease end in miscarriages vs. 6 percent of controls)
3. Adenovirus gastroenteritis (may be triggered in latent celiac disease that
initiates small bowel mucosal pathology)
4. Addison's disease (see Autoimmune diseases below)
5. AIDS (progression reflected by anti-gliadin Ab levels)
6. Albumin and prealbumin, serum (both low in CD)
7. Alkaline phosphatase, serum and bone (both elevated in CD)
8. Alopecia areata (both patchy and universal prevalence may be as high as
1 out of 85 celiacs, almost 3,000 times higher than predicted)
9. Amenorrhea (38 percent of celiacs vs. 9.2 percent of controls)
10. Anemia, folic acid deficiency, and iron deficiency, (along with elevated liver
enzymes, one of the two most common laboratory abnormalities observed
Appendix
in celiac disease; 6 percent of premenopausal women with anemias of unknown cause biopsy-proven celiac disease)
11. Anorexia nervosa/atypical eating disorders
12. Aphthous stomatitis/canker sores (up to 25 percent of celiac patients may
have a history of oral ulceration)
13. Arthropathies (26 percent of CD patients with arthritic symptoms;
41 percent if still eating gluten vs. 7.5 percent of controls):
a. Arthritis, undifferentiated
b. Arthralgia
c. Polyarthritis, seronegative
d. Juvenile arthritis
e. Rheumatoid arthritis
14. Asperger's syndrome
15. Asthma
16. Ataxia
17. Atopic disorders:
a. Allergic rhinitis
b. Asthma
c. Eczema
d. Chronic urticaria
18. Attention deficit disorder (ADD)
19. Attention deficit hyperactivity disorder (ADHD)
20. Autism
21. Autoantibodies associated with celiac disease:
a. IgA anti-gliadin antibodies
b. IgG anti-gliadin antibodies
c. IgA antiendomysium antibodies (autoantigen recently identified as the
enzyme intestinal transglutaminase):
d. IgA (and IgG) antireticulin antibodies
e. Anti-transglutaminase IgA and IgG autoantibodies
f Anti-gastric inhibitory peptide (GIP) cell antibodies
g. Anti-duudenal secretin cell autoantibodies
h. Anti-enteroglucagon cell autoantibodies
Comprehensive List of Gluten-Associated Medical Conditions
(89
i. Anti-thyroid microsomal autoantibodies
j. Anti-thyroid peroxidase autoantibodies (27 percent positive)
k. Anti-gastric parietal cell autoantibodies
1. Anti-adrenal cortex (suprarenal) autoantibodies
m. Anti-pancreatic islet cell autoantibodies
n. Anti-cardiolipin (14 percent of all CD patients)
0. Anti-single-stranded DNA (14 percent of all CD patients)
p. Anti-double-stranded DNA autoantibodies (23 percent)
q. Anti-mitochondrial antibodies
r. Cardiac-specific autoantibodies (in some cases of idiopathic dilated cardiomyopathy—see below)
s. IgG anti-cell adhesion molecule desmoglein 3 in pemphigus vulgaris
22. Autoimmune diseases:
a. Insulin-dependent diabetes mellitus (10 percent of all celiacs develop
IDDM, up to 8 percent of IDDM patients have or will develop celiac
disease; many authorities are now recommending that all IDDM patients be screened for CD annually for several years after IDDM diagnosis)
b. Hyperthyroidism (3.7 percent of all celiacs) and hypothyroidism
(8 percent of all celiacs); some authorities are now recommending that
all autoimmune thyroid patients be routinely screened for celiac disease)
c. Hypoparathyroidism
d. Inflammatory bowel disorders
e. Idiopathic Addison's disease
f. Alopecia areata
g. Vitiligo
h. Systemic lupus erythematosus (SLE)
1. Celiac disease (CD)
j. Chronic active hepatitis
k. Biliary cirrhosis, primary
1. Dermatomyositis
m. Pemphigus vulgaris (oral, esophageal, and anal lesions)
190
Appendix
n. Myasthenia gravis
0. Autoimmune polyendocrine syndrome:
1. Hashimoto's thyroiditis with IDDM
2. Dermatitis herpetiformis with IDDM
p. Sjogren-Larsson syndrome
q. IgA nephropathy (Berger's disease)
23. Axonai neuropathy
24. Berger's disease/IgA nephropathy (Berger's is 6 times more frequent in
males—5 percent of all primary glomerular diseases in United States,
10 to 20 percent in Europe, 30 to 40 percent in Asia]
25. Biliary cirrhosis, primary (autoimmune disease with antimitochondrial
antibodies; primarily disease of women)
26. Biliary duct atresia (30 percent incidence in childhood CD)
27. Bone diseases:
a. Osteoporosis/lowered bone density in kids and adults
b. Osteopenia
c. Osteomalacia
d. Bone pain, "growing pains" in children
e. Bone fractures, pathological (from osteomalacia)
f. Elevated bone alkaline phosphatase
g. Hyperparathyroidism, secondary
h. Hypoparathyroidism, magnesium-deficiency induced
1. Elevated serum osteocalcin
j. Elevated urinary hydroxyproline excretion
k. Hypocalcemia
1. Hypocalcuria
28. Breast-feeding, absence of (up to 80 percent of CD children are not
breast-fed, 96 percent breast-fed for 2 months or less)
29. Bullous pemphigoid
30. Calcium deficiency
3 1. Cancers:
a. Adenocarcinoma of small intestine
b. B-cell lymphoma
c. Bladder cancer
Comprehensive List of Gluten-Associated Medical Conditions
d. Brain cancer
e. Prostate cancer
f. Squamous cell carcinoma of pharynx and esophagus
g. T-cell lymphoma of small intestine (31 to 100 times more frequentlyfound in celiac patients; new cases of non-Hodgkin's lymphoma are
increasing by a little over .5 percent per year and deaths by 1.8 percent
per year)
h. Testicular cancer
32. Cardiomyopathy, idiopathic dilated (in children, 25 percent mortality rate
the first year after diagnosis)
33. Celiac disease (CD):
a. Classical active CD (gluten gastroenteropathy)
b. Silent CD/subclinical gluten intolerance (typical CD mucosal histology with no abdominal symptoms)
c. Latent CD (normal mucosa with positive serology initially; villous
atrophy, mucosal crypt hyperplasia, intraepithelial lymphocyte infiltration develop later)
d. Abortive type CD (transient/non-permanent—development of gluten
tolerance later on)
e. Potential CD
f. CD in first-degree relatives (4.5 to 8.5 percent overall, 13.8 percent of
siblings, 12 percent of offspring of celiacs, 70 percent of identical twins)
34. Cerebellar atrophy/cerebellar syndrome
35. Cerebral atrophy (central, cortical, and/or cerebellar)
36. Cerebral calcification (mostly occipital region)
37. Cerebral syndromes:
a. Epilepsy
b. Cerebral calcification
c. Headache
d. Mental deterioration
e. Visual disturbances
38. Chest pain, noncardiac (see Esophageal symptoms)
39. Cholangitis, primary sclerosing
40. Cholecystokinin (CCK) inhibition (reduced CCK release from duode-
192
Appendix
num with subsequent reduction in gallbladder emptying and pancreatic
secretions)
41. Cirrhosis, primary biliary
42. Colitis, microscopic (27 percent with villous atrophy, 17 percent with
CD-related serology, most with HLA-DQ genetic marker)
43. Crohn's disease
44. Cutaneous vasculitis
45 Dementia, intellectual impairment
46. Dental enamel lesions, permanent teeth (96 percent of CD children and
83 percent of CD adults with celiac-type color and structural defects, horizontal grooves, and/or vertical pits on one or more permanent teeth)
47. Depressive illness ("Depression is the most common symptom of gluten
intolerance")
48.
Dermatitis herpetiformis (classical non-GI manifestation of celiac disease;
25 percent without villous atrophy or crypt hyperplasia; instead only minor mucosal changes seen)
49.
Diabetes mellitus, insulin-dependent (2.6 to 7.8 percent of IDDM children have CD—including silent and latent CD, 10 to 100 times higher
prevalence of CD than expected)
50.
Diarrhea, chronic
Down syndrome (prevalence of CD detected is 1 in 14)
51. Duodenal ulcers (antibiotic resistant)
52. Dysarthria
53 Dyslexia
54, Dysphagia (45 to 50 percent of CD patients—see Esophageal symptoms;
55. when associated with iron deficiency, is called the Paterson-Brown Kelly
(Phimmer-Vinson] syndrome)
56 Eczema
57, Edema (in the more ill CD patients)
58. EEG abnormalities (may persist for 1 year on gluten-free diet)
59 Emotional and behavioral disorders:
a. Irritability
b. Querulousness, petulance
c. Impulsivity
Comprehensive List of Gluten-Associated Medical Conditions
d. Depression (common presenting symptom of CD)
e. Anxiety
f. Aggressiveness
g. Autism
h. ADHD
i. Schizophrenia
60. Epilepsy:
a. Epilepsy associated with cerebral calcifications
b. Epilepsy associated with migraine headaches
c. Epilepsy associated with hyperactivity
d. Epilepsy associated with myoclonic ataxia (Ramsay Hunt's syndrome)
61. Esophageal symptoms (dysphagia, dysmotility, reflux esophagitis, heartburn, noncardiac chest pain)
62. Esophagitis, reflux (see Esophageal symptoms)
63. Eustachian tube dysfunction
64. Exorphin/opioidlike activity (gluten-induced)
65. Facial and hair features typical of CD:
a. Blue eyes and fair hair
b. Triangular-shaped face with prominent forehead and narrow jaw
c. Premature graying
66. Failure to thrive
67. Family members of celiac patients (parents and siblings)
68. Fatigue, chronic
69. Flatulence
70. Folic acid deficiency
71. Food sensitivities (soy, milk, monosodium glutamate, e.g.)
72. Gallbladder malfunction (impaired emptying, poor bile delivery, gallstones, e.g.)
73. Gastric inhibitory polypeptide reduction (inhibition of gut hormone release from upper small intestine)
74. Gastric ulcers
75. Gastrointestinal bleeding, occult (X-ray negative)
76. Gastrointestinal disorders:
a. Abdominal pain (up to 25 percent of CD patients complain of pain)
194
Appendix
b. Irritable bowel syndrome
c. Crohn's disease
d. Ulcerative colitis
e. Chronic diarrhea
£ Steatorhea
g. Recurrent aphthous ulcers [canker sores)
h. Nausea and vomiting
i. Bloating, abdominal distension
j. Flatulence
k. G1 bleeding
% Angular stomatitis
m. Macroglossia
n. Gastric ulcers
o. Abnormal intestinal permeability (leaky gut)
p. Pancreatic insufficiency
q. Gut hormone inhibition (secretin, CCK, e.g.)
r. Dyspepsia, esophageal reflux (5 percent of all such patients with gluteninduced duodenal villous atrophy)
77. Gastrointestinal polypeptide inhibition:
a. Choiecystokinin
b. Gastric inhibitory polypeptide
c. Secretin
78. Genetics (see Human leukocyte antigens [HLA] below)
79. Glomerulonephritis, IgA-mediated
80. Grave's disease
81. Gynecological disorders:
a. Amenorrhea
b. Delayed menarche
c. Delayed puberty
d. Early menopause
82. Hair abnormalities:
a. Alopecia areata
b. Premature graying
Comprehensive List of Gluten-Associated Medical Conditions
9
83. Headaches (persistent, recurring, migrainelike, often not responsive to conventional therapies)
84. Heartburn (see Esophageal symptoms)
85. Heart disease:
a. Ischemic heart disease, lower incidence of death in CD
b. Cardiomyopathy, idiopathic dilated
c. Chest pain, noncardiac (see Esophageal symptoms)
d. Pericarditis, recurrent
86. Hematuria (macroscopic or microscopic)
87. Hepatitis, chronic active
88. Hepatitis, nonspecific reactive
89. Hormonal/endocrine abnormalities:
a. Elevated plasma testosterone
b. Reduced plasma dihydrotestosterone
c. Elevated luteinizing hormone
d. Hyperprolactinemia (associated with lowered CNS dopamine levels,
a marker for active CD)
e. Hyper- or hypoparathyroidism (associated with bone disease)
f. Hypo- or hyperthyroidism
g. Growth hormone deficiency
h. Reduced secretin gut hormone blood levels
90. Human leukocyte antigens: HLA-DR3, DQ2, and B8 positive haplotypes
(frequency of HLA-DR3 antigens in patients with CD is about 88 percent; normal population only 44 percent); HLA-DR3 and especially DQ2
antigens in diseases are thought to be associated with celiac disease:
a. Celiac disease
b. Dermatitis herpetiformis
c. Multiple sclerosis
d. Down syndrome
e. Insulin-dependent diabetes mellitus (DR3 and B8 present in 86 percent
of patients with both CD and IDDM; IDDM alone, 41 percent)
f. Grave's disease
g. Idiopathic Addison's disease
196
Appendix
h. Sicca syndrome
i. Systemic lupus erythematosus
j. Idiopathic IgA membranous nephropathy
k. Myasthenia gravis
91. Hypertransaminasemia, alanine and aspartate (9 percent of ail cases of
hypertransaminasemia of unknown origin; found in about 50 percent of
all celiac patients still on a gluten-containing diet; often found in otherwise symptom-free celiacs; returns to normal on gluten-free diet)
92. Hypoalbuminemia (in untreated celiac disease; returns to normal with a
gluten-free diet)
93. Hypocalcemia
94. Hypocomplementemia
95. Hypogonadism
96. Hypoperfusion, frontal cortex of brain
97. Hyposplenism (10 percent of CD adults; remits on gluten-free diet)
98. IgA deficiency, total serum (3 percent frequency in both CD and IDDM
vs. approximately 0.2 percent in normal population)
99. IgA nephropathy (see Nephropathies)
100. IgG and/or IgA anti-gliadin antibodies elevation (serum)
101. Impotence/loss of libido (19 percent of CD males are impotent)
102. Infertility in both women and men (2.1 million U.S. married couples are
infertile—one-third male, one-third female, one-third both; 18 percent
of all celiac males are infertile; abnormal sperm is reversed; a 50 percent
increase in conception rate occurs on strict gluten-free diet)
103. Intellectual impairment/mental deterioration
104. Intraepithelial gamma/delta T-lymphocytes (increased density in mucosal epithelium)
105. Iron deficiency anemia (of unknown origin—very common in celiac
patients)
106. Irritable bowel syndrome (IBS)
107. Ischemic heart disease (lower rate of death in CD patients)
108. Kidney disease (see Nephropathies)
109. Lactose intolerance (found in 50 percent of celiac patients)
Comprehensive List of Gluten-Associated Medical Conditions
110. Leaky gut syndrome/abnormal intestinal permeability
111. Lipofuscin storage (increased deposition in nerves, skin, and muscles)
112. Liver disease (15 times more frequent in CD; 47 percent of CD adults
and 57 percent of CD children have evidence of
UveT impairment; biopsy-
proven liver damage has been reported in most untreated CD patients):
a. Abnormal function tests (elevated transaminases common extraintestinal sign of CD)
b. Biliary cirrhosis
c. Chronic active hepatitis
d. Nonspecific reactive hepatitis
113. Lupus erythematosus (0.3 to 1.3 percent of all CD patients)
114. Lymphocyte reactivity (reduced against tumors in CD)
115. Lymphocytic colitis (authorities recommend routine screening for CD)
116. Lymphocytic gastritis
117. Lymphomas (31 to 100 times more common in CD patients; risk returns
to near normal withfive years on a gluten-free diet)
118. Macroglossia (enlargement of the tongue)
119. Magnesium deficiency
120. Malabsorption:
a. Low hemoglobin
b. Reduced mean corpuscular volume (MCV)
C. Low vitamin B l 2
d. Low folic acid
e. Chronic diarrhea, flatulence
f. Weight loss with wasting
g. Chronic fatigue
121. Malabsorption syndrome (chronic diarrhea, flatulence, weight loss, and
fatigue)
122. Malignancies (see both entries: Cancers and Lymphomas)
123. Malnutrition (deficiencies in iron, zinc, calcium, magnesium, potassium,
and vitamins Bg, B 12 , folic acid, A, D, E and/or K)
124. Mast cell degranulation
125. Menarche, delayed (delayed by over 1 year)
198
Appendix
126. Menopause, early (occurs 2-4 years earlier in CD patients)
127. Mental symptoms and disorders:
a. Inability to concentrate
b. Mental deterioration
c. Mental lethargy
d. DistractibiJity
e. Intelligence deficits
£ Dementia
g. Down syndrome
h. ADHD
i. ADD
j. Autism
k. Schizophrenia
128. Mesangial IgA deposits (often associated with celiac disease, Crohn's
disease, adenocarcinomas, dermatitis herpetiformis, psoriasis, or IgA
nephropathy)
129. Microscopic colitis (see Colitis)
130. Mineral deficiencies:
a. Iron deficiency
b. Calcium deficiency (hypocalcemia)
c. Zinc deficiency
d. Magnesium deficiency (hypomagnesemia)
e. Potassium deficiency (hypokalemia]
f. Selenium deficiency
131. Miscarriages
132. Mortality (a 1.9- to 3.4-fold increased mortality overall in adults—but
not children, asymptomatic relatives, or those diagnosed by serology;
death occurs most frequently withinfirst to third year following diagnosis and then declines over time; highest death rates between ages 45-54
for men and 55-64 for women; major reported cause is intestinal lymphoma):
a, A 31- to 100-fold increased risk of death from small intestinal
lymphomas
b. An 8.5-fold increased risk of deathfrom esophageal cancer
Comprehensive List of Gluten-Associated Medical Conditions
c. A 2.3-fold increased risk of death from all other malignant disease in
CD men
d. Chronic liver disease
e. Lower death rate from ischemic heart disease and strokes than normal
population
133. Multiple sclerosis
134. Myasthenia gravis
135. Mycosis fungoides
136. Myoclonic ataxia, progressive
137. Natural killer cell (reduced count)
138. Nephropathies:
a. IgA nephropathy (Berger's disease)
b. IgA glomerulonephritis
c. Nephrotic syndrome
d. Proteinuria
139. Neurological conditions, chronic, of unknown cause:
a. Ataxia/myoclonic ataxia
b. Axonal neuropathy
c. Brain atrophy
d. Cerebellar atrophy/cerebellar syndrome
e. Epilepsy
f. Hypoperfusion, frontal cortex
g. Intellectual deterioration
h. Multiple sclerosis
i. Optic neuropathy
j. Paresthesia
k. Peripheral neuropathy
1. Polyneuropathy
m. Progressive neuromyopathy
n. Ramsay Hunt's syndrome (epilepsy with myoclonic ataxia)
140. Obstetrical disorders:
a. Recurrent abortions
b. Stillbirths
c. Infertility
200
Appendix
d. Subfertility
e. Reduced time span of fertility
f. Reduced pregnancy rate
141. Ocular myopathy
142. Opioidlike activity
143. Optic neuropathy
144. Osteocalcin elevation (serum)
145. Osteomalacia
146. Osteoporosis/osteopenia (70 percent of untreated CD patients with low
hone density; in patients unresponsive to standard therapies—estrogen,
vitamin D, calcium, bisphosphonates, calcitonin; bone density increases
by 7.7 percent in 1 year on strict gluten-free diet alone)
147. Otitis media
148. Palmoplantar pustulosis (skin condition of soles and palms)
149. Pancreaticobiliary diseases:
a. Pancreatic insufficiency
b. Pancreatitis
c. Papillary stenosis
d. Papillitis
e. Chronic duodenitis
f. Impaired cholecystokinin release
150. Paresthesia
1 b 1. Pericarditis, recurrent
152. Pervasive developmental disorder
153. Polyarthritis, seronegative
154. Polymyositis
155. Polyneuropathy
156. Presenile dementia
157. Prolactin, elevated
158. Proteinuria (see Nephropathies)
159. Psoriasis
160. Psychiatric symptoms:
a. Depression (common presenting symptom in celiac patients)
b. Anxiety
Comprehensive List of Gluten-Associated Medical Conditions
161. Puberty, delayed
162. Ramsay Hunt's syndrome (epilepsy with myoclonic ataxia)
163. Rheumatoid arthritis (see Arthropathies)
164. Sarcoidosis (1.8 percent of all CD patients)
165. Secretin release inhibition (a 9-fold difference between untreated celiac
and non-celiac following intraduodenal stimulation with HC1)
166. Secretory IgA deficiency (2.6 percent of CD patients are IgA deficient,
10 to 16 times higher than general population)
167. Selenium deficiency
168. Sexual behavior disorders (in untreated CD):
a. Decreased frequency of sexual intercourse
b. Decreased satisfaction from sexual intercourse
169. Short stature/growth failure (bone and growth retardation in children;
celiac disease is a more common factor here than primary growth hormone deficiency)
170. Sicca syndrome
171. Sjogren-Larsson syndrome (2.9 percent of all CD patients and 15 percent of all Sjogren's patients with biopsy-proven celiac disease)
172. Skin diseases-.
a. Bullous pemphigoid
b. Chronic urticaria
c. Cutaneous vasculitis
d. Dermatitis herpetiformis
e. Eczema
f Psoriasis
g. Palmoplantar pustulosis
173. Sperm abnormalities (reversed on gluten-free diet):
a. Oligospermia (reduced sperm count)
b. Abnormal sperm motility
c. Abnormal sperm morphology
174. Steatorrhea
175. Stillbirths
176. Suicide
177. Thrombocytopenic purpura
202
Appendix
178. Thyroid disease, autoimmune (up to 13 pcrcent of all CDs; subclinical
thyroid disease may be reversed in some cases within 1 year on glutenfree diet):
a. Hypothyroidism (found in 5.8 to 8 perent of all celiac patients)
b. Hyperthyroidism (found in 3.7 to 5 percent)
179. Turner's syndrome (a chromosomal disease associated with autoimmune
disorders including thyroid disease, inflammatory bowel disease, diabetes, and juvenile rheumatoid arthritis; all overrepresented in celiac
disease)
180. Ulcerative colitis
181. Urticaria (hives)
182. Vasculitis
183. Villous atrophy (partial/subtotal and total)
184. Vitamin deficiencies:
a. Vitamin A deficiency
b. Vitamin Bf i deficiency
c. Vitamin B,, deficiency
d. Folic acid deficiency
e. Vitamin D deficiency
f. Vitamin E deficiency
g. Vitamin K deficiency (associated with nosebleeds, easy bruisabiiity,
internal hemorrhaging, and bone loss)
185. Vitiligo
186. Weight loss/failure to gain weight
187. Zinc deficiency
APPENDIX E
Heroic Thinkers and
Dietary Biases
Several heroic thinkers and researchers have blazed the trail past our cultural
biases and preconceived notions. Their thoughtful observations and insightful interpretations of the health implications of gluten have opened the path to new insights that may help avert an epidemic in the offing for the twenty-first century.
The stories of these courageous individuals have helped shape tomorrow's world
of medicine. If we look at the evidence objectively, we can learn from them today.
STANISLAS TANCHOU ( 1 7 9 1 - 1 8 5 0 )
Stanislas Tanchou was a visionary French physician who campaigned with Napoleon
at Waterloo, then settled in Paris to practice medicine and do research. He conducted what may be thefirst detailed statistical study of the incidence of cancer
deaths. He accumulated and analyzed data detailing the causes of death for people
in Paris and surrounding rural areas over a period of eleven years. He also examined information about cancer found in ancient Egyptian mummies, along with
204
Appendix
information that was then current from Egypt and Algiers. Tanchou's published
findings over 150 years ago offer the first published evidence that implies that
foods from grains contribute to cancer.
Tanchou offered the prophetic observation that "cancer is like insanity, found
most often in the most civilized countries . . ."
VLLHJALMUR STEFANSSON
(1879-1962)
Another early researcher, an anthropology instructor at Harvard University
named Vilhjalmur Stefansson, was one of the few to pay attention to Tanchou's
ideas. His research, observations, deductions, and references regarding cancer are
what led us to Tanchou's work. Stefansson left his teaching position in 1906 and
traveled to the north coast of Canada to live among the Eskimos. He lived and
worked among the Inuit, immersed in their way of life, for eleven of the twelve
years between 1906 and 1918. Stefansson looked for but found no sign of cancer
in the Stone-Age culture of the Inuit. He was thefirst to report on the healthfulness of this high-fat, high-animal protein diet in 1913. We would add that it was
what the Inuits were not eating that also protected them from cancer; namely,
the absence of gluten cereals.
Stefansson was also there to record the devastating loss of that protection, following adoption of a Western diet by these genetically ill-prepared northern natives. His observations, subsequent investigations, and their synthesis resulted in a
theory of cancer that may hold the answer, even a cure, for many cancer patients.
His theory is summarized in the title of his book, Cancer: Disease of Civilization!,
and stands unchallenged. Cancer is a genetically influenced environmental disease
of civilization.
SAMUEL G E E AND R . A . GIBBONS
In 1888, Dr. Samuel Gee provided a highly regarded, detailed description of classical celiac disease. One of Gee's contemporaries, R. A. Gibbons, believed this disease to be rare, afflicting only children. According to Gibbons, patients' either
recovered from this disease of childhood or they died. In either case, there would
be little reason to look for it in adults.
Sadly, Gibbons's very narrow perspective and Gee's focus on the most dra-
Heroic Thinkers and Dietary Biases
205
matic cases resulted in perspectives that were to dominate medical thinking for
more than a century. Even today, many U.S. practitioners still consider only childhood celiac disease to be a serious malady.
WHEAT-CELIAC C O N N E C T I O N AND WILLEM KAREL DICKE
(1905-1962)
One of the greatest visionaries of the twentieth century was Dr. W. K. Dicke. His
courageous pursuit of the underlying cause of celiac disease was a giant step
toward recognition of the real nature of this disease. He invested much of his
professional career to the solution of the celiac puzzle.
Dicke first began to suspect wheat as the cause of celiac disease when the
mother of one patient suggested that possibility in 1932. Dicke stated'. "As one
frequently comes across the unfavorable influence of these nutrients, the conviction gradually grew within me that the observation mentioned above [that wheat
might be the cause of celiac disease] was not any chance occurrence peculiar to a
certain individual, but had something to do with the presence of celiac disease."
It is particularly interesting that Dicke says, when talking about bread, biscuits,
and starches, that they are frequently seen as having an unfavorable influence.
This original insight led to the monumental discovery that gluten is requisite to
the manifestation of celiac disease.
Although there is some debate as to when Dr. Dickefirst realized that wheat
caused celiac symptoms, the evidence clearly indicates that he had done so by
1936. In keeping with a disgraceful tradition of attacking and abusing original
thinkers going back countless centuries, Dr. Dicke was mocked and ridiculed
when he tried to present hisfindings at a 1950 conference of gastroenterologists
in New York City.
It was not until it became possible to confirm Dicke'sfindings through intestinal biopsies that his discovery began the agonizingly slow process of being accepted as the treatment of choice for celiac disease. The wheat-celiac connection,
despite compelling evidence in support of it, continued to be a matter of debate
in medical literature until 1964.
Unfortunately, some elements of the debate have continued outside the literature. There are dermatologists today who continue to treat the skin manifesta-
206
Appendix
tion of celiac disease, called dermatitis herpetiformis, by prescribing steroid medications and/or dapsone instead of recommending a gluten-free diet. These drugs
usually control the most obvious symptoms of this condition but do not address
the cause. The dermatologists using this approach argue that it is unusual for patients to comply with a gluten-free diet, so the medication makes more sense. We,
of course, vehemently disagree with this position, pointing to the increased risk of
many cancers and autoimmune diseases and the protective benefits offered by a
gluten-free diet.
SCHIZOPHRENIA C O N N E C T I O N AND
F. CURTIS D O H A N
[1908-1991)
Medical science took yet another leap forward when Dr. F. Curtis Dohan
learned that schizophrenia is frequently found in people with celiac disease, and
celiac disease is frequently found in people with schizophrenia. Dohan was a
prominent medical teacher, internist, and researcher who worked most of his illustrious forty-year career in the Philadelphia area. He has more than eighty publications in scientific journals to his credit, Dohan also enjoyed reading mystery
stories, an interest that would ultimately benefit humanity. He found the association between schizophrenia and celiac disease intriguing. He pursued this medical puzzle with the same joy and interest that he used to solve the who-done-its
in his leisure reading. His dogged pursuit of the schizophrenia-celiac connection
is the wellspring of a whole new understanding of diet-induced mental illness,
and his work serves as a mode! for investigating other dietary ailments.
In 1969, Dohan and his colleagues conducted an experiment. They reported
significant improvements in hospitalized schizophrenic patients following a glutenfree and dairy-free diet. This report generated quite a lot of skepticism, but the results were soon repeated by M. Singh and S. Kay. The Dohan group'sfindings were
repeated. Dohan subsequently conducted investigations showing that when
gluten-containing grains are rare, schizophrenia is also rare.
In 1979, the discovery of morphinelike substances in partly digested gluten
proteins, called gliadorphins or gluteomorphins, supported Dohan's work from a
completely different direction. These morphinelike substances have been shown
to interfere with the immune system, impact on blood vessel dilation, and alter
chemical activity- in the brain, thus acting as contributing factors in many psychi-
Heroic Thinkers and Dietary Biases
207
atric and brain illnesses, including learning and attention disorders, major depression, sleep disorders, postpartum psychosis, and autism.
AUTISM C O N N E C T I O N , PAUL SHATTOCK, AND KALLE REICHELT
Dr. Paul Shattock was a plant biochemist and lecturer at the University of Sunderland when his son was diagnosed with autism in 1974. He began collecting
data on autism research. Then, Shattock heard speculation that autism is the result of peptide poisoning, following on Dohan's work. He began investigating the
possibility that gluten and dairy were at the root of his son's ailment, and he has
contributed important research that supports this hypothesis.
Dr. Kalle Reichelt, a researcher at the Pediatric Research Institute in Oslo,
Norway, was also investigating peptides from gluten and dairy products in autistic patients. By 1990, Reichelt and Shattock had discovered that 90 percent of the
autistic patients they studied had abnormally high levels of urinary peptides that
they surmised were from dairy and gluten cereals.
These men, and now many other researchers, have established a connection
between gluten consumption and several types of mental illness, behavioral problems, and learning disabilities. Broader recognition of these discoveries is slow.
Given adequate time, we are confident that this work will become universally accepted. However, many concerned parents and others will want to act more
quickly on this information, as the appropriate diet is very safe and nutritious. There
is no downside to this therapy other than the inconvenience of implementing it
while ensuring optimal nutrition. Those who currently suffer from these conditions will be unlikely to benefit from this information if they await its general acceptance before changing their diet.
N O N - G L U T E N AGENTS OF DISEASE AND LOREN CORDAIN
Recent research conducted by Loren Cordain is also making headway in a broader
area of gluten research. Cordain, a researcher at Colorado State University, has
taken a more global approach to the evaluation of the impact of consuming
gluten-containing grains. He has reported several antinutrients, psychoactive substances, and other non-gluten agents discovered in cereals, all of which can damage the human intestinal wall.
Cordain has also presented information about how we have made dramatic
208
Appendix
changes to the human diet since beginning cultivation of cereal grains ten thousand years ago and how those changes are now threatening to overwhelm us with
chronic disease. Cordain has also debunked several myths regarding the diets of
hunter-gatherers, showing that they were likely much more dependent on animal
protein and fats than was previously believed.
All of these pioneering scientists, along with others too numerous to mention,
have expanded human knowledge in this arena. Because of their diligence and
considerable courage to think originally in the face of rejection and mockery,
humanity is now offered an important choice.
The twentieth century's development of widespread consumption of highly
processed foods brought with it a dramatic increase in gluten consumption. Examine the "ingredients" label on almost any processed food so you may see for
yourself. Gluten and/or its derivatives are usually present. The view that these
foods are healthy or at least not harmful helps to maintain many of the traditional
forms of gluten consumption. Together, these and other factors have created the
unprecedented level of gluten gluttony with which the industrial world entered
the twenty-first century.
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INDEX
Absorption, 93
Active transport, 139
Addiction, and celiac disease, 111-12
Additives, 101-2
Agriculture, 23-24
Alcoholism, ] 50
Amaranth, 180
and gluten sensitivity, 122
liver disease, 127
model for dietary treatment of, 131-32
and molecular mimicry, 119-22
reversal/prevention with gluten-free
diet, 176
rheumatoid arthritis, 128-30
thyroid disease, 123
American Journal of Clinical Nutrition, 137
Amino acids, 29, 119
Animal protein, 20-22, 87-88
Bacterial translocation, 32
Antibodies, 30, 68-70, 117, 119, 129,
Bakeries, 104
146-47, 165,176
Barley, 25-26
Anti-gliadin antibody (AGA) blood test, 68
Behavior, 148
Arginine, 29
Beverages, 89
Attention deficit disorder (ADD), 149
Bleeding, 55
Atypical celiac disease, 39-40
Blood testing, 15, 28, 40, 47, 67
Autism, 153-57, 207
anti-gliadin antibody, 68
Autoimmune diseases and gluten, 117-18,
endomysium antibody, 70-71
132-33
IgA antibody, 70
connection to gluten, 118-19
importance of AGA tests, 68-70
diabetes, 124-27
tissue transglutaminase antibody, 71-72
found in celiac disease, 131, 186'
Bone-building, 139, 142
240 Index
Bone density, 24, 139, 141, 143
Bone density testing, 80-81
Bones, 137-38
Bowel diseases and gluten, 160-61
Crohn's disease, 164-65
enteritis, 165
intestinal infections, 164
irritable bowel syndrome (IBS),
162-63
microscopic and ulcerative colitis, 166
position on gut disease, 166-68
swollen lymph glands, 166
Brain disorders and gluten, 144
anti-gluten antibodies that attack the
brain, 146-47
autism, 153-57
epilepsy, 152-53
ergotism, 147-48
gluten s effects on mental health,
144-45
mood, behavior, psychology, 148-52
multiple sclerosis, 157-59
range of neurological effects of gluten,
145-46
Brain size, 24
Bruising, 55
Bulk bins, 104
B vitamins, 54, 97-98
Calcium, 81, 94-95, 137-40
Cancer, 40, 43, 60, 105-6, 115-16, 131
and addicts, 111-12
exorphins and development of, 110
gluten increases risk of 109
hazards of opiate use in, 113
and insulin abnormalities, 115
limits of our knowledge of, 106-7
and malabsorption, 114
rates of in celiac disease, 113-14
what we know about, 107-9
Carbohydrates, 93
Casein, 113-14
Casomorphins, 114
Celiac disease, 3-4, 36, 162,170
and addiction, 111-12
applying research in to gluten sensitivity,
45-46
atypical, 39-40
autoimmune diseases found in, 186
classic, 37-39
deaths from, 27
follow-up, 15-17
latent, 40-41
and malabsorption, 11-13, 114
new knowledge of, 9-12
and osteoporosis, 138-40
ranges of sensitivity in, 43-45
rates of cancer in, 113-14
rectal challenge for diagnosing, 72-74
redefinition of, 12-13
research advances, 13
signs and symptoms of 181-82
silent or asymptomatic, 40
small intestinal biopsy for diagnosing,
63-65
symptoms, shift in, 6-7
treatment, 14-15
wheat connection, 205-6
Celiac sprue, 44
Chimpanzee diet, 20
Chromium deficiency, 126
Cirrhosis, 127
Citrus fruits, 88
Classic celiac disease, 37-39
Codex Aliment a ri us, 102-3
Coffee, 89
Collagen, 136
Comfort foods, 23, 109
Contamination sources, 103-4
Cordain, Loren, 31, 207-8
Corn, 88
Coughing, 55-56
Counseling, 79
Cow's milk, 35
Crohn's disease, 164-65
Cross-reactivity. See Molecular mimicry
Cruciferous vegetables, 86
Dairy foods, 2, 5,88, 113, 125
Dapsone, 85
Delayed-onset food sensitivities, 88-89
Delayed-type hypersensitivity, 32-33
Denmark, 26-27
Dental work, 82
Depression, 148
Dermatitis herpetiformis, 41-43, 75
Desensitization therapies, 83
Detoxification, 78
Diagnosis, 15
Dicke, Willem Karel, Dr., 12, 205-6
Dietary protein, 29-30
Digestion, 29-30
Disaccharides, 66
DNA analysis, 27
Index 241
Dohan, F. Curtis, Dr., 151, 156, 206-7
Donaldson, S. S., Dr., 114
Double-blind crossover, 173
Downregulation, 131
Down syndrome, 60
DQ2, 28
DQ8, 28
Duhring's disease. See Dermatitis
herpetiformis
Dyslexia, 150
Eggs, 87-88
Elastin, 171
Endomysium antibodies, 93
Endomysium antibody (EMA) test, 70-71,
73, 172
Endoscopy, 64
Enteritis, 108, 165
Enzymes, 30
Epilepsy, 152-53
Epitope, 119
Ergotamine, 151-52
Ergotism, 147-48
Esophageal reflux, 54
Essential fatty acids, 87
Essential nutrients, 29
Exorphins, 23, 109-10
Eye exams, 82
False positive anti-gliadin tests, 41
Family tree, 58, 60
Fats, 86-87,93
Fertile Crescent, 178
Fine, Kenneth, Dr., 63
Fish, 87
Fistulas, 164
Folate, 53
Follow-up, 15-17
Food allergies, 16, 80, 119, 164-65, 179
Food guide pyramid (USDA), 6, 135
Food labeling, 102-3
Food storage, 23
Food supply changes, 34-35
Fruits, 86
Fu, 102
Gee, Samuel, Dr., 11-12, 204-5
General adaptation syndrome, 8
Genetics, 27
Genetic testing, 75-76
Germs, 175-76
Gibbons, R. A., Dr., 11,204-5
Gliadin antibodies, 3, 26,30, 127, 165, 171
Glucose-tolerance testing, 81
Glutamine, 29, 176-77
Gluten
addictive nature of, 16, 78-79
and autoimmune diseases, 118-33
and bowel diseases, 160-68
and brain disorders, 144-59
disease process in body, 2-3
and germs, 175-76
hidden sources of, 183-85
increased risk of cancer from, 109
medical conditions associated with,
187-202
and osteoporosis, 134-43
in pharmaceutical products, 84
trace quantities of, 83-84
and viruses, 175
Gluten challenge, 65-66
Gluten-free diet, 9, 16, 76-77, 131-32,
163
benefits o£ 179
dietary dangers, 99-104
dietary supplements, 92-99
informed aftercare, 79-82
nutritional cautions, 82-85
optimal nutrition on, 85-92
physical addiction to gluten, 78-79
reversal/prevention of autoimmune
diseases with, 176
sample menu, 90
Gluten-free household, 80
Gluten grains, 3
Glutenin, 26, 171
Gluten sensitivity, 2, 27, 33, 164-65
applying celiac disease research to,
45-46
and autoimmune disease, 122-33
non-celiac, 5-6
redefining, 13-14
tolerance of] 7-9
Gluten sensitivity testing, 61-76, 178
Gluteomorphin, 146
Grains
evolution of, 24-26
genetics of, 27
and hunter-gatherers, 22
mismatch with people, 18-19
natural selection, 19-22
Roman, spread of, 26-27
switch to agriculture, 23-24
undigested, 30
242
Hadjivassiliou, M., Dr., 14
Hallucinations, 152
Heartburn, 54
Hepatitis, 127
Heroic thinkers, 203-8
Heroin addicts, 111-12
High-risk groups, 56-60
Hip fractures, 135, 137
HLA-B8, 28
HLA-DQ2, 63
HLA-DQ8, 63
HLA (human leukocyte antigens), 14, 28,
62
Homocysteine, 53
HPP, 102
Hunter-gatherers, 22,114
HVP, 102
Hyperglycemia, 81
Hypocalcemia, 94
Hypothalamic-pituitary-adrenal (HPA)
axis, 110
IgA antibodies, 70, 176
IgA dermatosis, 75
IgG antibodies, 58, 68-70, 176
IgG ELISA blood test, 73, 80
Immune system, 2-3
and cancer, 110
delayed-type hypersensitivity of 32-33
HLA proteins of 28
and molecular mimicry, 1 19
Infertility, 28
Inflammation, 30
Insulin, 88
Insulin abnormalities, 115
Insulin-dependent diabetes mellitus
(IDDM), 120, 124-27, 176
Internal animal organs, 87-88
Intestinal biopsy, 12-13, 172
Intestinal infections, 164
Intestinal lining, 31
Intestinal permeability, 30, 32, 34, 78, 91,
120, 130, 158
Iron, 96-97
Iron deficiency, 53
Irritable bowel syndrome (IBS), 162-63
Italy, 177-78
Karolus, Herbert, Dr., 150
Lancet, 157
Latent celiac disease, 40-41
Index
Leaky gut, 30, 32, 34, 78, 91, 120, 158,
176-77
sugar-absorption test for identifying,
66-67
Learning problems, 150
L-glutamine, 176-77
Liver disease, 127
Liver-function testing, 81-82
Low blood pressure, 54
Low-cholesterol diet, 87
LSD, 152
MacDougall, Roger, 157
Magnesium, 93-94, 1 3 9 ^ 0
Malabsorption, 11-13, 114
Marsh, Michael N., Dr., 14, 46, 64, 72
Marsh system, 64-65
Matheson, Norman, Dr., 157-58
Matthews-Larson, Joan, 150
Meat, 87
Medical history, 54-56
Meillon, Ross, 58, 60
Memory cells, 119-20
Menu, sample, 90
Microscopic colitis, 166
Middle-ear disease, 5
Migraine headaches, 151-52
Mineral deficiencies, 55
Molecular mimicry, 119
conditions needed to activate,
121-22
and germs, 121
problem with circulating gluten
antibodies, 120-21
Mood, 148
MSG, 102
Mucosa, 31
Mullis, Kary, 21
Multiple food allergies, 88-89
Multiple sclerosis, 125-26, 157-59
Murray, Joseph, Dr., 162
Myelin sheath, 125, 159
Natural killer cells, 110, 131
Natural selection, 19-22
New knowledge, 9-12
New perspectives, 174-80
Non-celiac gluten sensitivity, 5-6, 41,
162
Non-gluten disease agents, 31, 207-8
Northern grains, 25-26
Nutrient deficiencies, 114
Index
Oats, 3, 99-100, 163
Obesity, 52
Oils, 86-87
Omega-3 oils, 87, 92
Omega-6 oils, 87
Omega-9 oils, 87
Opiates, 110, 113
Opioids, 78, 109-10, 131
Organic foods, 86
Osteoblasts, 139, 142
Osteocalcin, 136
Osteomalacia, 141
Osteoporosis, 143
bones as living tissue, 137-38
causes of in celiac patients, 138-40
defined, 138
and gluten, 134-35
gluten, vitamins, and bone health, 136-37
impact of aging and sex hormones on
bone health, 142
in non-gluten sensitive, 136
osteomalacia and gluten, 141
and parathyroid gland, 140-41
Paradigm shifts, in research, 174-80
Parathyroid gland, 93-94, 139-41
Peanuts, 88
Peptides, 29-30, 78, 148
Phosphorous deficiency, 139
Phytate, 136
Placebo effect, 172
Population screening, 177-78
Potassium, 97
Poultry, 87
Pro-grain beliefs, 18-19
Progress, in research, 170
Protein, 2-3, 20-22, 87-88
Psoriasis, 132
PTH, 139
Quercetin, 86, 89
Quinoa, 180
Randolph, Theron, Dr., 150
Reading, Chris, Dr., 9, 58, 60, 114
Rectal challenge, 72-74
Reichelt, K. L., Dr., 155-56, 207
Research, 169-70
future, 170-72
new perspectives and paradigm shifts,
174-80
problems with current methods, 172-74
243
Researchers, 203-8
Respiratory allergies, 55-56
Restaurant cards, 91-92
Rheumatoid arthritis, 128-30
Rice, 180
Risk factors, 47
high-risk groups, 56-60
medical history, 54-56
obesity, 52
regular medical checkups, 52-54
self-examination questions, 48-51
short stature, 51-52
Roman grain, 26-27
ROME criteria, 162
Rotation diet, 91
Rye, 25-26, 163
Rye molds, 147
Schizophrenia, 145, 151-52, 206-7
Seafood, 88
Seizures, 152-53
Selective advantage, 20-22
Selenium, 95-96
Self-examination questionnaire, 48-51
Selye, Hans, 7-8
Senility, 145-46
Seven Weeks to Sobriety (MatthewsLarson), 150
Shattock, Paul, Dr., 156, 207
Shellfish, 87
Shortness of breath, 55-56
Short stature, 24, 51-52
Silent/asymptomatic celiac disease, 40
Skin biopsy, 75
Small intestinal biopsy, 63-65
Soda, 89
Soy, 88,125
Spices, 86
Spina bifida, 60
Stefansson, Vilhjalmur, 204
Steroids, 84-85
Storage proteins, 26
Sugar, 88
Sugar-absorption test, 66-67
Supplements, 92-99
Support groups, 79-80
Swollen lymph glands, 166
Symptom chasing, 174
Tanchou, Stanislas, 203-4
Tea, 89
Teenagers, 88
244 Index
Testing for gluten sensitivity, 6]
answers found in 11LA-DQ markers,
62-63
blood testing, 67-72
genetic testing, 75-76
gluten challenge, 65-66
gfuten-free diet for testing positive, 76
HI,A markers, 62
rectal challenge, 72-74
skin biopsy, dermatitis herpetiformis,
and IgA dermatosis, 75
small intestinal biopsy, 63-65
sugar-absorption test, 66-67
Theories, 169
Thyroid disease, 123
Thyroid testing, 81
Tissue transglutaminase (tTG) antibody
test, 71-72
TPP, 102
Treating the cause, 174
TVP, 102
Type I diabetes, 81
Type 2 (non-insulin-dependent) diabetes,
126-27
Ulcerative colitis, 166
Undigested grain proteins, 30
USDA food guide pyramid, 6, 135
Vaccinations, early, 34
Vegetables, 86
Villi, 63-64
Villous atrophy, 176-77
Viruses, 175
Vitamin A, 98
Vitamin A deficiency, 137
Vitamin B s , 97-98
Vitamin B ] 2 , 9 2
Vitamin C, 92, 136
Vitamin C deficiency, 55
Vitamin D, 99, 139, 141
Vitamin E, 98-99
Vitamin K deficiency, 55, 136-37
Wakefield, Andrew, 155
Warning signs, 52-54
Water, 89
Western diet, 65
Wheat, 2, 25-26,35, 163, 205-6
Wheat starch, 100-101
Wheezing, 55-56
Wild game, 87
Withdrawal, 78
Work history, 58
Yeast, 88
Your Family Tree (Meillon & Reading), 60
HEALTH/NUTRITION
Could
gluten
contrib
to you
chroni
illness?
Bread makes up more than half of the total
daily calories in the average diet of people in
most countries, and grains represent more
than one-third of all food crops grown worldwide. Yet the protein contained in various
bread grains, gluten, contributes to long-term
illness for millions of people. While the USDA
recommends that we obtain a majority of our
calories from cereal grains, it is precisely these
grains that can incite life-threatening celiac disease and chronic gluten sensitivity.
In Dangerous Grains, a renowned food allergy expert an
patient advocate come together to reveal for the first time
gluten grains on chronic illness. James Braly and Ron Hoggan
our current understanding of gluten sensitivity and celiac
explore the impact of wheat, rye, barley, spelt, kamut, tritica
grains on a range of conditions—cancer, autoimmune diseas
sis, and intestinal disease, among many others. Tracking th
evolutionary history of humans and grain consumption, this
you understand how grains can affect your health, and wheth
risk for gluten-influenced illness.
James Braly, M.D., is an expert in food allergies and glut
During his twenty years of clinical and research experience,
develop, implement, and popularize food allergy testing and
screening among physicians throughout the United States. Dr
self gluten-sensitive.
Ron Hoggan, M.A., was diagnosed with celiac disease in 19
quent research on the disease and the gluten grains that provo
published in numerous newsletters and journals, and on m